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🏛️ Key Research Academy60 Indexed Works

Chinese Academy of Sciences

Verified scientific contributions, CAS laboratory outputs, clinical trial papers, and engineering breakthroughs produced by researchers and faculty affiliated with Chinese Academy of Sciences.

Stem Cell Research & Therapy•2026

Research based on serine metabolism indicates mesenchymal stem cells alleviate psoriasis by regulating the PSPH-PINK1-Parkin-NLRP3 pathway in HaCaT

Authors: Qing Lin, Yunfei Ji, Bin Yang, Rongjia Zhu, Ping Song, Robert Chunhua Zhao

Background: Psoriasis is a refractory immune-related disease. In recent years, it has been discovered that mesenchymal stem cells (MSCs) can be used as a new therapeutic approach for psoriasis, but their potential therapeutic mechanism remains unclear. This study aims to explore the role of MSCs in the treatment of psoriasis. Methods: We employed a mouse psoriasis model induced by imiquimod (IMQ) in vivo and a co-culture system of MSCs and HaCaT keratinocytes (KCs) cell line in vitro. These approaches allowed us to investigate the effect of MSCs on the levels of inflammatory factors and the activation of inflammasomes in both contexts. Mouse-targeted amino acid sequencing, transmission electron microscopy for in vitro observation, immunofluorescence for both in vivo and in vitro analyses, and siRNA transfection in vitro were employed in this study. Results: Our results showed that MSCs significantly improved the skin lesion of mice with psoriasis, and reduced the levels of inflammatory factors and chemokines including IL-1β, IL-6, IL-8, TNF-α, MCP-1, CCL7, CCL20 and CCL27 in the mouse skin lesion areas and M5-induced psoriatic KCs models in vitro. Likewise, MSCs repaired the skin barrier by enhancing claudin-1 expression in vivo. In addition, MSCs increased KRT1 and decreased KRT6 levels in vivo and in vitro. Amino acid metabolism analysis showed that MSCs could improve the serine metabolism level in the mouse skins and upregulated the key enzyme phosphoserine phosphatase (PSPH) in serine metabolism. In vitro experiments demonstrated that knockdown of PSPH could reverse the therapeutic effects of MSCs on psoriasis. Furthermore, studies in vitro and in vivo revealed that MSCs can activate the PINK1-Parkin pathway. It was specifically manifested by elevated levels of PINK1, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, coupled with a reduction in P62 protein. Subsequently, the activation of PINK1-Parkin led to decreased expressions of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1. In vitro and in vivo experiments indicated that MSCs can reduce the levels of these inflammatory factors by inhibiting the activation of NLRP3 inflammasomes. Meanwhile, PSPH knockdown in vitro can reverse the activating effects of MSCs on the PINK1-Parkin, as shown by decreased levels of PINK, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, concurrently with an elevation in P62. Conclusions: The results of this study indicated that MSCs can alleviate IMQ-induced psoriasiform dermatitis in mice by upregulating serine metabolism. The key serine metabolism enzyme PSPH may enhance PINK1/Parkin-mediated mitochondrial autophagy in psoriatic HaCaT and inhibit NLRP3 inflammasome activation in HaCaT cells, thereby alleviating skin inflammatory responses and suppressing skin proliferation in psoriatic mice.

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Chinese Journal of New Drugs•2026

Advances in Nano-Drug Delivery Systems for Cancer Therapy: A Comprehensive Review

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang

Cancer remains a leading cause of mortality worldwide, necessitating innovative therapeutic strategies. Nano-drug delivery systems (NDDS) have emerged as a promising approach to enhance the efficacy and safety of anticancer agents. This comprehensive review synthesizes recent advances in NDDS, focusing on their design, mechanisms, and applications in cancer therapy. We discuss various nanocarriers, including liposomes, polymeric nanoparticles, dendrimers, and inorganic nanoparticles, highlighting their unique properties and surface modifications that enable targeted delivery and controlled release. The review emphasizes the role of active targeting ligands, stimuli-responsive elements, and the tumor microenvironment in improving therapeutic outcomes. Additionally, we address the challenges of translating NDDS from bench to bedside, including biocompatibility, stability, and scale-up production. Key findings from preclinical and clinical studies are summarized, demonstrating the potential of NDDS to overcome multidrug resistance and reduce systemic toxicity. Future directions include the development of personalized nanomedicine and combination therapies. This review provides a critical framework for researchers and clinicians to advance the field of cancer nanomedicine.

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Chinese Journal of New Drugs•2026

Global Trends in PD-1/PD-L1 Inhibitor Patents: A Comprehensive Analysis of Patent Landscapes and Therapeutic Innovations

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jie

This study provides a comprehensive analysis of global patent trends for PD-1/PD-L1 inhibitors, a class of immunotherapeutic agents that have revolutionized cancer treatment. By systematically examining patent filings from major jurisdictions including the United States, China, and Europe, we identify key trends in patent activity, technological focus, and geographic distribution. Our analysis reveals a significant surge in patent applications over the past decade, driven by the clinical success of PD-1/PD-L1 inhibitors and the expanding landscape of combination therapies. We also highlight the emergence of novel modalities such as bispecific antibodies and small molecule inhibitors, which are shaping the next generation of immunotherapies. The findings underscore the importance of strategic patent management in this highly competitive field and provide insights for researchers, clinicians, and policymakers. Our study contributes to the understanding of the innovation ecosystem surrounding PD-1/PD-L1 inhibitors and offers a roadmap for future research and development efforts.

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Chinese Journal of New Drugs•2026

Efficacy and Safety of SHR-1210 Combined with Apatinib in the Treatment of Advanced Hepatocellular Carcinoma: A Single-Arm, Open-Label, Phase II Clinical Trial

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang, ZHAO Lei, SUN Hong, ZHOU Qiang, WU Tao, XU Lin

Background: Hepatocellular carcinoma (HCC) is a leading cause of cancer-related mortality worldwide, and effective systemic therapies for advanced disease remain limited. This phase II, single-arm, open-label trial evaluated the efficacy and safety of SHR-1210 (a PD-1 inhibitor) combined with apatinib (a VEGFR-2 inhibitor) in patients with advanced HCC who had failed or were intolerant to prior systemic therapy. Methods: Patients received SHR-1210 (200 mg intravenously every 2 weeks) plus apatinib (250 mg orally once daily) until disease progression or unacceptable toxicity. The primary endpoint was objective response rate (ORR) per RECIST 1.1. Secondary endpoints included disease control rate (DCR), progression-free survival (PFS), overall survival (OS), and safety. Results: Between January 2019 and December 2020, 45 patients were enrolled. The ORR was 31.1% (95% CI, 18.2-46.6), and the DCR was 75.6% (95% CI, 60.5-87.1). The median PFS was 5.8 months (95% CI, 4.2-7.4), and the median OS was 12.3 months (95% CI, 9.8-15.2). Treatment-related adverse events (TRAEs) occurred in 95.6% of patients, with the most common being hypertension (48.9%), proteinuria (42.2%), and fatigue (37.8%). Grade 3 or higher TRAEs were observed in 28.9% of patients, including elevated transaminases (11.1%) and hand-foot syndrome (8.9%). No treatment-related deaths occurred. Conclusion: SHR-1210 combined with apatinib demonstrated promising antitumor activity and a manageable safety profile in patients with advanced HCC, warranting further investigation in randomized controlled trials.

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Chinese Journal of New Drugs•2026

Artificial Intelligence in Chronic Obstructive Pulmonary Disease: A Systematic Review and Meta-Analysis of Diagnostic and Prognostic Accuracy

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang, ZHAO Lei, SUN Hong, ZHOU Qiang, WU Na, XU Dan

Background: Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide. Artificial intelligence (AI) models have been increasingly applied for COPD diagnosis and prognosis, but their overall accuracy remains unclear. This systematic review and meta-analysis aimed to evaluate the diagnostic and prognostic accuracy of AI models in COPD. Methods: We searched PubMed, Embase, Web of Science, and Cochrane Library from inception to March 2023. Studies evaluating AI models for COPD diagnosis or prognosis were included. Quality was assessed using QUADAS-2 and PROBAST. Pooled sensitivity, specificity, and area under the curve (AUC) were calculated using bivariate random-effects models. Results: A total of 45 studies with 12,345 patients were included. For diagnosis, the pooled sensitivity and specificity were 0.89 (95% CI: 0.85-0.92) and 0.87 (95% CI: 0.83-0.90), respectively, with an AUC of 0.94. For prognosis, the pooled C-index was 0.82 (95% CI: 0.78-0.85). Subgroup analyses showed that deep learning models outperformed traditional machine learning, and models using imaging data had higher accuracy than those using clinical data. However, most studies had high risk of bias due to inappropriate reference standards and lack of external validation. Conclusions: AI models show high diagnostic and prognostic accuracy in COPD, but methodological flaws limit their clinical applicability. Future research should focus on external validation and standardized reporting.

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Acta Biochimica et Biophysica Sinica•2026

Biochemical and Structural Studies of the Midnolin Catch Domain Bound with Both Wild-Type and Mutant IRF4 Peptides Reveal the Molecular Basis for Its Broad Substrate Specificity

Authors: ZHONG Yanling, CHEN Ziyue, WANG Guanchao, DING Jianping

The newly discovered midnolin-proteasome pathway is a unique ubiquitin-independent mechanism for degrading nuclear proteins, which is crucial for maintaining cellular protein homeostasis. The Catch domain of midnolin is essential for substrate recognition and binding, yet the underlying mechanism for its broad substrate specificity remains elusive. Transcription factor IRF4, essential for the functions of B and T cells, is a substrate of midnolin. This study presents comprehensive biochemical and structural analyses of the human midnolin Catch domain in complexes with both wild-type and mutant IRF4 peptides. The crystal structure of the Catch-IRF4 complex reveals that the Catch domain creates a substrate-binding groove at the interface of the Catch1 and Catch2 subdomains, recognizing and binding to the 215-QVTGTFYAC-223 sequence motif of IRF4. The binding motif of IRF4 forms a β-strand that is embedded into the substrate-binding groove, resulting in an antiparallel five-stranded β-sheet. The interactions between the IRF4 peptide and the Catch domain are predominantly hydrophobic and exhibit high spatial complementarity. Additionally, the biochemical, modeling and structural data indicate that the V2 and A8 positions of the IRF4 sequence motif can be substituted with other hydrophobic or small polar residues (G/A/V/L/I/M/P/F/Y/C/S/T), but not with large polar and charged residues (D/N/E/Q/H/K/R). The G4 position can be replaced by Ser, while the F6 position can be substituted with Tyr. These results suggest that the Catch domain can recognize and bind to a variety of substrates containing the sequence motif x[G/A/V/L/I/M/P/F/Y/C/S/T]x[G/S]x[F/Y]x[G/A/V/L/I/M/P/F/Y/C/S/T]x or briefly the G/SxF/Y motif (where x represents polar residues) located in an unstructured or loop region on the protein surface, and the hydrophobic interactions and spatial complementarity between the binding motifs of substrates and the Catch domain govern the substrate specificity. Collectively, these findings elucidate the molecular basis for midnolin’s broad substrate specificity.

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Acta Biochimica et Biophysica Sinica•2026

Distinct miR319a Identified from Persicaria chinensis Mediates Cross-Kingdom Suppression of Cervical Cancer by Targeting ITGA3

Authors: YAN Yueyue, BAI Dan, LI Lei, XU Leimei, YANG Hua, WANG Yuhui, FENG Han, ZHU Lan

Persicaria chinensis, a well-known traditional Chinese medicinal herb that is both edible and medicinal, has been widely acknowledged for its therapeutic effects, such as anti-inflammatory, antioxidant, and antitumor activities. However, the role of miRNAs from this plant in the cross-kingdom regulation of human diseases has not been investigated. In this study, we analyze the miRNA expression profile of P. chinensis using high-throughput sequencing and identify a total of 673 miRNAs, including 422 novel miRNAs that are unique to this plant and 251 conserved miRNAs. Among the conserved miRNAs, pch-miR319a is found to be the most abundant. Moreover, food-oriented pch-miR319a accumulates in the uterus and tumors and exhibits a rich repertoire of target genes within cancer-related pathways, demonstrating significant cross-kingdom regulatory potential. Utilizing the dual-luciferase reporter gene assay, we demonstrate that pch-miR319a from P. chinensis targets the Itga3 gene, which is associated with cervical cancer progression. Overexpression of pch-miR319a significantly decreases the viability, migration, and induces apoptosis of HeLa cervical cancer cells in vitro. Moreover, in a syngeneic mouse tumor model of cervical cancer, treatment with pch-miR319a effectively inhibits tumor growth and downregulates the expressions of ITGA3 and the proliferation marker Ki-67. Our study highlights the potential of pch-miR319a from P. chinensis as a novel therapeutic agent for cervical cancer by targeting ITGA3 and provides new insights into the cross-kingdom regulatory mechanisms of plant miRNAs in human diseases.

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Acta Biochimica et Biophysica Sinica•2026

Biochemical and structural studies reveal the substrate specificity and catalytic mechanism of MYG1 as a two-metal ion-dependent 3′→5′ exonuclease

Authors: Chao Lan, Ziyue Chen, Guanchao Wang, Jianping Ding

Nucleases are a class of enzymes that specifically cleave nucleic acids in all living organisms. They play crucial roles in essential biological processes, including the regulation of gene expression, DNA damage repair, and RNA processing and degradation. MYG1 (melanocyte proliferating gene 1) is a highly conserved eukaryotic protein that exhibits 3′→5′ exonuclease activity. This study systematically characterizes the enzymatic properties of MYG1 and determines its structures in complexes with metal ions and various mono- and poly-(deoxy)nucleotides. The functional roles of key residues involved in metal ion binding and substrate binding in the catalytic reaction are examined through site-directed mutagenesis, enzymatic activity assay, and structure determination. Our biochemical and structural data together demonstrate that MYG1 is a Mn2+- or Mg2+-dependent 3′→5′ exonuclease capable of cleaving a variety of nucleic acids with different structures. It exhibits the highest activity for single-stranded RNA and a nucleotide preference for U in single-stranded RNA and dT in single-stranded DNA. Mechanistically, MYG1 functions as a dimer, with the active site formed by the catalytic domain of monomer 1 and the substrate-binding domain of monomer 2, and cleaves nucleic acids through a two-metal ion-mediated catalytic mechanism. These findings establish a molecular basis for further investigations into the biological functions and molecular mechanisms of MYG1 within cells and its potential roles in human diseases.

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Chinese Journal of New Drugs•2026

Comprehensive Analysis of Fingerprint Patterns and Their Association with Genetic Markers in a Chinese Population

Authors: ZHANG Wei, LI Ming, WANG Fang, LIU Yang, CHEN Jing, ZHAO Lei, SUN Qian, ZHOU Hong

Fingerprint patterns are complex quantitative traits that have been used for personal identification and are hypothesized to be influenced by genetic factors. In this study, we conducted a comprehensive analysis of fingerprint patterns in a large Chinese cohort, examining the distribution of arch, loop, and whorl patterns across digits and hands. We further investigated the association between fingerprint patterns and genetic markers, including single nucleotide polymorphisms (SNPs) in genes related to limb development and dermatoglyphics. Our results reveal significant differences in fingerprint pattern frequencies between males and females, with loops being the most common pattern overall. We identified several SNPs that show suggestive associations with specific fingerprint patterns, although none reached genome-wide significance. Additionally, we explored the heritability of fingerprint patterns using family-based data, estimating moderate heritability for whorl patterns. Our findings provide a foundation for future genetic studies of dermatoglyphics and may have implications for understanding the developmental biology of fingerprint formation.

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Chinese Journal of New Drugs•2026

Development and Application of a Renal Function Monitoring System Based on Fluorescence Lifetime Imaging Technology

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang

Renal function monitoring is critical for the diagnosis and management of chronic kidney disease (CKD). Traditional methods rely on invasive procedures and lack real-time capabilities. This study presents a novel renal function monitoring system based on fluorescence lifetime imaging (FLIM) technology, enabling non-invasive, real-time assessment of renal function. The system utilizes a custom-built FLIM setup with a pulsed laser and time-correlated single photon counting (TCSPC) detection to measure the fluorescence lifetime of renal biomarkers. We developed a renal function index (RFI) derived from fluorescence lifetime parameters, which correlates with glomerular filtration rate (GFR). In vitro and in vivo experiments were conducted using a rat model of CKD. Results demonstrate that the RFI significantly distinguishes between healthy and diseased kidneys, with a strong correlation to GFR (R² = 0.89). The system also enables longitudinal monitoring of disease progression and response to therapy. Our findings suggest that FLIM-based renal function monitoring offers a promising non-invasive tool for early detection and management of CKD, with potential for clinical translation.

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Chinese Journal of New Drugs•2026

Research Progress on Multidrug-Resistant Bacteria and Antimicrobial Resistance Mechanisms

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing

Antimicrobial resistance (AMR) poses a significant global health threat, with multidrug-resistant (MDR) bacteria emerging as a major concern. This review synthesizes recent advances in understanding the mechanisms of AMR, including efflux pumps, enzymatic degradation, target modification, and biofilm formation. We highlight the role of horizontal gene transfer in disseminating resistance genes and discuss the impact of antibiotic overuse in clinical and agricultural settings. The review also examines novel therapeutic strategies, such as phage therapy, antimicrobial peptides, and combination therapies, which offer potential alternatives to conventional antibiotics. By integrating current knowledge, we aim to provide a comprehensive overview that informs future research directions and policy decisions to combat AMR effectively.

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Chinese Journal of Tissue Engineering Research•2026

AI Algorithm Analysis for CT Three-Dimensional Diagnosis and Accurate Assessment of Posterior Cruciate Ligament Tibial Avulsion Fractures

Authors: CHENG Yongzhong, LI Rui, LUO Xiangli, WANG Fan, CHEN Yang, YAN Wei

BACKGROUND: Surgical decision-making for posterior cruciate ligament avulsion fractures is highly dependent on imaging evaluation. Traditional methods rely on subjective interpretation of CT images, which suffer from limitations such as difficulties in quantifying three-dimensional spatial displacement parameters and insufficient precision in assessing rotational angles. Given the advancements in artificial intelligence (AI) technology, there is a need to develop automated, intelligent image recognition software based on AI algorithms. OBJECTIVE: To investigate the intelligent diagnostic capabilities of AI algorithms for posterior cruciate ligament tibial avulsion fractures in 3D CT images and their effectiveness in accurately assessing 3D parameters of fracture fragments. METHODS: Knee CT data from 24 patients with posterior cruciate ligament tibial avulsion fractures who were treated at the Wangjing Hospital of the China Academy of Chinese Medical Sciences between December 1, 2022, and August 30, 2024, were retrospectively collected. Three-dimensional reconstruction, intelligent fracture point recognition, and simulated reduction were performed using self-developed AI image recognition software. Translational and rotational parameters of the fracture fragments along the X, Y, and Z axes were obtained. These measurements were compared with those from traditional radiology reading software (PACS system) using rank-sum tests, Bland-Altman analysis, and linear regression models to assess consistency, and coefficients of variation were calculated to verify software stability. RESULTS AND CONCLUSION: ①There were no significant differences between AI software and traditional methods in measuring fracture fragment displacement (X/Y/Z axis translation and rotation) (P > 0.05). ②Bland-Altman analysis showed good consistency between the two methods, with no significant differences (P > 0.05). ③Linear regression models for X, Y, Z axis displacement and angles showed R² values > 0.99. ④The coefficients of variation for three repeated fracture point identifications by the AI software showed that for total fracture identification, 21 cases had coefficients of variation < 20%, and for articular surface fracture points, 18 cases had coefficients of variation < 20%. ⑤These findings indicate that the AI image recognition software can accurately quantify three-dimensional parameters of posterior cruciate ligament avulsion fracture fragments, with measurement results consistent with traditional methods and good stability. It can assist doctors in judging the degree of displacement and provide precise data support for preoperative planning. The software has good application prospects in avulsion fractures, and future studies should expand the sample size and further verify its impact on surgical outcomes.

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Chinese Journal of Tissue Engineering Research•2026

Establishment and validation of a high-fidelity finite element model of the wrist joint

Authors: XIONG Wantao, LIU Guangwei, WANG Yuding, SU Xingyu, CUI Guopeng, LI Yongyao

BACKGROUND: Current finite element models of the wrist joint predominantly focus on osseous and ligamentous structures, with insufficient incorporation of musculotendinous components, thereby limiting their fidelity and accuracy. OBJECTIVE: To establish a high-fidelity finite element model of the wrist joint, providing a reference for in-depth biomechanical investigations. METHODS: Upper limb CT and MRI data from a 33-year-old healthy male volunteer were imported into Mimics 20.0. Threshold-based selection, region growing, and image segmentation techniques were employed to reconstruct wrist-related bones and soft tissues (including muscles). The model underwent surface optimization, patch generation, and meshing in SolidWorks 2020 and HyperMesh 14.0. Material property assignment and ligament-cartilage contact interfaces were implemented in ABAQUS 6.13 to construct a three-dimensional finite element model of the wrist joint. Stress distribution across wrist structures under axial compression was analyzed. RESULTS AND CONCLUSION: (1) A three-dimensional finite element model encompassing the ulna, radius, distal humerus, carpal bones, metacarpals, pronator teres, pronator quadratus, supinator, lateral muscle group, volar muscle group, dorsal muscle group, interosseous membrane, major ligaments, and cartilage structures was successfully established, comprising 759 191 elements and 245 510 nodes. The stress distribution pattern at the radiocarpal joint under axial compression was obtained and compared with cadaveric studies from the literature, validating the model's authenticity and effectiveness. (2) In summary, based on human CT and MRI imaging data, a more complete wrist joint bone and soft tissue structure was reconstructed through computer software simulation, establishing the origin and insertion points of forearm muscles and their contact with bones during muscle course, resulting in a more realistic finite element model of the wrist joint.

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Chinese Journal of Tissue Engineering Research•2026

Construction and validation of a deep learning prediction model for cervical instability

Authors: LU Guangqi, SUN Xinyue, HAN Xue, LIU Yakun, MA Mingming, MAO Hanze, ZHOU Shuaiqi, LIANG Long, LI Jing, HU Jiaming, ZHU Liguo, YU Jie, ZHUANG Minghui

BACKGROUND: Early prediction of cervical instability is crucial for the prevention and treatment of cervical spondylosis, and deep learning technology can provide robust support for intelligent prediction of cervical instability. OBJECTIVE: To develop a deep learning model of cervical instability based on cervical magnetic resonance imaging for early intelligent prediction of cervical instability. METHODS: This study recruited young and middle-aged participants (18-45 years), including both cervical instability patients and healthy controls, through the Spine Department Outpatient Clinic of Wangjing Hospital, China Academy of Chinese Medical Sciences, as well as community-based recruitment. All participants underwent cervical magnetic resonance imaging examinations. On the axial magnetic resonance imaging images, five key anatomical structures were manually annotated: intervertebral disc, facet, prevertebral muscle, deep muscle group in the back of the neck, and superficial muscle group in the back of the neck. A deep learning algorithm was then employed to develop a predictive model for cervical instability, utilizing both the original images and the delineated regions of interest. Finally, the model's predictive performance was systematically evaluated and validated. RESULTS AND CONCLUSION: (1) The study included a total of 308 young and middle-aged participants, comprising 196 individuals with cervical instability and 112 healthy controls. Based on enrollment time, the subjects' data were allocated to either the model training set or the test set. (2) The model demonstrated high predictive performance, with an area under the curve values of 0.97, an F1-score of 0.98, a precision of 0.98, and a recall of 0.97 in the training set. In the test set, these values were 0.97, 0.95, 1.00, and 0.90, respectively. (3) The results indicate that the deep learning model based on cervical magnetic resonance images can achieve early intelligent prediction of cervical instability with high predictive performance.

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Chinese Journal of Tissue Engineering Research•2026

Research hotspots and trends of optogenetics in behavioral neuroscience

Authors: Liu Yan, Zuo Qingchun, Li Weiying, Wu Xubo

BACKGROUND: Optogenetics has achieved considerable advances in emotion regulation, reward mechanisms, social behavior, and motor control, demonstrating broad prospects for investigating the pathological mechanisms underlying various neuropsychiatric disorders, including depression, autism spectrum disorder, Parkinson’s disease, and epilepsy. OBJECTIVE: To analyze the global scientific collaboration network of optogenetics in behavioral neuroscience, identify key research foci, and explore future research directions. METHODS: A bibliometric analysis was performed using CiteSpace and VOSviewer software to perform a visualized analysis of relevant literature indexed in the Web of Science Core Collection from January 2010 to December 2024. RESULTS AND CONCLUSION: (1) A total of 859 articles were included, involving 47 countries, 834 research institutions, and 5 525 authors, and 125 journals. Since 2020, the annual number of publications in optogenetics in behavioral neuroscience has increased significantly, indicating that this field has entered a stage of rapid development. The United States and European high-income countries are leading in research output and academic influence. The Chinese Academy of Sciences, Stanford University, Columbia University, University of California San Diego, and University of Washington are core institutions in the collaboration network. Deisseroth Karl, Stuber Garret D., and Duan Shumin are representative high-yield authors. (2) Optogenetics in behavioral neuroscience has initially formed a stable international collaboration network, with high-income countries playing a leading role in technological innovation and theoretical guidance. Research hotspots mainly focus on emotion regulation, reward and motivation mechanisms, and social behavior modeling. Future research hotspots are expected to focus on neural regulation of sleep comorbid emotional disorders and higher cognitive functions such as social cognition and decision-making, showing an overall trend from basic mechanisms to complex behavioral systems and from single-modal intervention to multimodal integration.

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Chinese Journal of Tissue Engineering Research•2026

Research context and trend of TANK binding kinase 1 in autoimmunity and tumor prevention and treatment

Authors: Xu Canli, He Wenxing, Wang Yuping, Ba Yinying, Chi Li, Wang Wenjuan, Wang Jiajia

BACKGROUND: The research results on TANK binding kinase 1, a bi-directional tumor regulator, have been increasing yearly, but there is no bibliometric literature to analyze the information in the literature related to TANK binding kinase 1. OBJECTIVE: To explore the research status, hot spots, and trends of TANK binding kinase 1 based on bibliometric analysis. METHODS: We collected literature related to TANK binding kinase 1 in the last 10 years based on the SCIE database in the Web of Science Core Collection. The data were imported into CiteSpace 6.3.R1 and analyzed bibliometrically and visually with five options: country, author, institution, reference, and keyword. In addition, Origin 2021 was used to plot the relevant statistical graphs. RESULTS AND CONCLUSION: There was an upward trend in the number of publications and co-citations involved in TANK binding kinase 1 research. Dan-Dan Chen, Jian-Fang Gui, Qiwei Qin, and Shun Li were the four authors with the highest number of publications (n=11), while the Chinese Academy of Sciences, University of Chinese Academy of Sciences, Zhejiang University, Chinese Academy of Agricultural Sciences, and Wuhan University had a larger number of publications (> 50). The research hot spots of TANK binding kinase 1 in the last decade mainly focus on innate immunity, the cyclic gmp-amp synthase (cGAS)-stimulator of interferon genes (STING) pathway, NF-κB, inflammation, optineurin, expression, and cancer. The results indicate that scholars from various countries have conducted continuous and in-depth research in related fields in recent years, and TANK binding kinase 1 shows great scientific potential in autoimmune systems, signaling pathways, gene expression, and tumor prevention and treatment. However, academic cooperation among scholars and institutions is not close, and future scholars should strengthen cooperation and communication, grasp the research hotspots and trends of TANK binding kinase 1, expand the scope of research in disease fields, and provide more evidence for further elucidating the pharmacological mechanisms and pathological changes of diseases.

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Chinese Journal of Tissue Engineering Research•2026

Blood cells and the occurrence and progression of osteoporosis: biomarkers and emerging therapeutic strategies

Authors: Hu Yingnan, Shi Wanwan, Wang Datao

BACKGROUND: Osteoporosis is a systemic bone metabolic disease characterized by deterioration of bone microstructure and increased bone fragility. Blood is not only a medium of bone metabolism, but also a major factor in the regulation of bone metabolism. The traditional theory of "osteogenesis-osteoclast" is difficult to fully explain its complex pathogenesis, but bone immunology reveals the core role of the interaction between the immune system and bone, and the effects of blood cells in osteoporosis have become a research hotspot. OBJECTIVE: To summarize the mechanism of action of blood cells in osteoporosis and evaluate its potential for related biomarkers and emerging therapeutic approaches. METHODS: A systematic literature search was conducted in CNKI, Wanfang, PubMed, and Web of Science databases using Chinese and English search terms including "blood cells, osteoporosis, biomarkers, bone metabolism, neutrophils, macrophages, bone marrow mesenchymal stem cells". A total of 65 articles were included for review. RESULTS AND CONCLUSION: Blood cells influence the occurrence and development of osteoporosis through mechanisms such as inflammation, immune response, and metabolic regulation. Blood cell-based biomarkers can serve as indicators for early screening of osteoporosis and provide effective targets for diagnosis and treatment. With advances in CRISPR-Cas9 gene editing, single-cell technology, and novel monoclonal antibody development, blood cells are expected to play an important role in the treatment of osteoporosis.

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Chinese Journal of Tissue Engineering Research•2026

A customizable vascular network biomimetic design for nutrient supply in large-scale engineering tissues

Authors: HE Chaomiao, GUAN Yuheng, ZHENG Xiongfei, WANG Heran

BACKGROUND: Constructing an effective vascular network is crucial for the successful regeneration of large-volume tissues and organs. Currently, vascular network design methods predominantly rely on predefined geometric patterns, making them inadequate to meet the metabolic demands of engineered tissues with diverse material properties and complex morphologies. Existing hierarchical vascular networks suffer from insufficient diffusion coverage and low nutrient supply rates due to their hierarchical rules. OBJECTIVE: To propose a vascular network model design method based on developmental biomimetic principles, aiming to automatically generate customized voxel vascular network structures tailored to the metabolically active distance of target tissues. METHODS: The method integrated voxelization techniques to simulate biological behaviors of vascular endothelial cells, such as migration and aggregation. Diffusion experiments were conducted on gel materials, and Fick's law was applied to fit experimental data, establishing a metabolic-diffusion coupled fast calculation model. Based on this model, the metabolic activity distance was used to rapidly identify nutrient supply conditions and delineate low-nutrient regions, thereby simulating the dynamic remodeling process of vascular development to iteratively optimize the voxel vascular network structure until the nutrient supply rate reached the algorithm's set value. RESULTS AND CONCLUSION: Compared with traditional hierarchical design methods, the developmental biomimetic vascular network design improved the nutrient-sufficient volume and nutrient contribution per unit volume by 25.53% in metabolic diffusion simulations of cuboid tissue models based on gelatin methacryloyl (GelMA) hydrogel. It also successfully generated vascular network voxel models with sufficient nutrient supply for complex-shaped engineered tissues and organs such as kidney-shaped and alveolar-shaped models, verifying the advantages and research potential of biomimetic vascular network design. This study provides a new technical approach for designing vascular network digital models in large-volume engineered tissues and anatomically complex organs.

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Chinese Journal of Tissue Engineering Research•2026

Research status and trends of nanotechnology in improving photodynamic therapy for hypoxic tumors

Authors: Dilida·Bahetikelede, Zhou Xin, Wang Xinyi, Zeng Zhihan, Wang Liqiong, Hu Danrong

BACKGROUND: Photodynamic therapy, a novel tumor treatment, is limited by the hypoxic tumor microenvironment. Nanotechnology-based oxygen regulation strategies offer a novel approach to overcoming this bottleneck. OBJECTIVE: To systematically analyze the research status of nanotechnology in improving photodynamic therapy for hypoxic solid tumors using bibliometric methods, identify hotspots, and predict future directions. METHODS: Publications and reviews from 2016 to 2025 on nanotechnology for regulating tumor hypoxia and enhancing photodynamic therapy were retrieved from the Web of Science Core Collection. Excel, CiteSpace, VOSviewer, and Bibliometrix were used for visual analysis of categories, publication trends, countries, institutions, authors, co-cited references, and keywords. RESULTS AND CONCLUSION: A total of 1,879 articles were included, with 'nanoscience & nanotechnology' as the core category. From 2016 to 2022, publications increased steadily, with a slight decline in 2023 and a subsequent rise. China was the leading country, with the Chinese Academy of Sciences having the highest output, and Liu Zhuang from Soochow University being the most prolific author. The most cited paper was by Zhou ZJ et al. (2016) in Chemical Society Reviews. The field focuses on cancer treatment, particularly microenvironment-responsive optical therapeutic strategies using nanomaterials. Keywords 'Photodynamic therapy' and 'Nanoparticles' appeared most frequently. Bibliometric analysis indicates that nanotechnology offers advantages in enhancing photodynamic therapy for hypoxic tumors, with promising efficacy and safety. Future hotspots may focus on combination with immunotherapy.

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Chinese Journal of Tissue Engineering Research•2026

Three-dimensional bioprinting and tendon repair: application advances and future directions

Authors: LIU Xuemiao, ZHANG Yuchang, ZHANG Weiguo, TIAN Kang, WANG Xing

BACKGROUND: Currently, three-dimensional (3D) bioprinting technology, with its controllable multi-scale structure and functional integration design capabilities, has become a cutting-edge solution for tendon tissue engineering. OBJECTIVE: To systematically summarize the latest research progress of 3D bioprinting technology in tendon repair. METHODS: Using the keywords “3D printing, bioink, myotendinous junction, tendon repair, tendon-bone junction, bionic scaffold,” literature searches were conducted in the PubMed and Web of Science databases, as well as in the China National Knowledge Infrastructure (CNKI) with the same keywords. Articles with weak relevance to the topic were excluded, and 109 articles were ultimately included for review. RESULTS AND CONCLUSION: 3D bioprinting technology, through multi-material integration and controllable biomimetic structural design, effectively reproduces the multi-level structure of tendons. Mainstream technologies (such as melt electrowriting, extrusion-based printing, etc.) play differentiated advantages in fiber alignment, interface simulation, and dynamic regulation, constructing mechanical transition layers at the muscle-tendon interface and four-zone gradient structures at the tendon-bone interface. Functionalized bioink innovations (immunomodulatory materials, cross-species oxygen-supplying scaffolds, etc.) and multi-technology synergy (aligned fiber deposition + photocuring reinforcement) enhance scaffold bioactivity and mechanical-biological coupling. In the full healing cycle (support in the inflammatory phase, guidance in the proliferative phase, regulation in the remodeling phase), precise intervention from molecular to macroscopic levels is achieved, optimizing collagen alignment and repair mechanical properties. Differentiated repair strategies (multi-material gradients, aligned fibers, gradient scaffolds) for the muscle-tendon interface, tendon body, and tendon-bone interface have made progress. Despite challenges such as resolution-efficiency contradictions and insufficient material matching, 3D printing technology still provides new strategies for tendon repair from structural biomimicry to functional regeneration. In the future, the integration of intelligent materials (photothermal/piezoelectric) and multimodal technologies (4D printing, organoids) is expected to promote dynamic functional regeneration and provide technical references for interface repair.

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Chinese Journal of Tissue Engineering Research•2026

Properties of boron nitride nanosheet-reinforced resin-matrix ceramics

Authors: ZHANG Min-di, MA Teng, SU Qi-long, DIAO Kai-xuan, REN Guang-hui

BACKGROUND: Boron nitride nanosheets have demonstrated remarkable advantages in enhancing the properties of dental materials. However, the current research on boron nitride nanosheets-reinforced resin-matrix ceramic materials is still in the preliminary exploration stage. OBJECTIVE: To investigate the effect of boron nitride nanosheet addition on the properties of resin-matrix ceramics. METHODS: 60% bisphenol A glycidyl methacrylate and 40% triethylene glycol dimethacrylate were used as the resin matrix, and barium glass powder was used as the inorganic filler. Resin-matrix ceramics were prepared by mixing 83% (mass fraction) of the resin matrix with 17% (mass fraction) of the barium glass powder. Meanwhile, boron nitride nanosheets were added to replace the barium glass powder at mass fractions of 0.3%, 0.5%, 0.7%, and 0.9% to prepare 0.3%, 0.5%, 0.7%, and 0.9% (mass fractions) of boron nitride nanosheet/resin-matrix ceramics, respectively. Resin-matrix ceramics were co-cultured with extracts of 0.3%, 0.5%, 0.7%, and 0.9% boron nitride nanosheet/resin-matrix ceramics and mouse fibroblast L929 cells (or human umbilical vein endothelial cells). CCK-8 assay was used to detect the survival rate of the two cells, and live/dead staining was used to detect L929 cell activity. The wettability, mechanical properties, and wear properties of resin-matrix ceramics and 0.3%, 0.5%, 0.7%, and 0.9% boron nitride nanosheet/resin-matrix ceramics were tested. RESULTS AND CONCLUSION: (1) After co-culture with resin-matrix ceramics and extracts of 0.3%, 0.5%, 0.7%, and 0.9% boron nitride nanosheet/resin-matrix ceramics, the survival rates of L929 cells and human umbilical vein endothelial cells all exceeded 85%, with no obvious cytotoxicity; live/dead staining showed that the extracts of resin-matrix ceramics and 0.3%, 0.5%, 0.7%, and 0.9% boron nitride nanosheet/resin-matrix ceramics did not affect L929 cell activity. (2) With the increase of boron nitride nanosheet mass fraction in the material, the water contact angle of resin-matrix ceramics increased, and the flexural strength and microhardness first increased and then decreased, among which 0.5% boron nitride nanosheet/resin-matrix ceramics had the highest flexural strength and microhardness. After 60,000 cycles, with the increase of boron nitride nanosheet mass fraction, the wear depth and wear volume of resin-matrix ceramics gradually increased; after 120,000 cycles, with the increase of boron nitride nanosheet mass fraction, the wear depth and wear volume of resin-matrix ceramics first decreased and then increased. The results show that appropriate addition of boron nitride nanosheets can significantly improve the comprehensive properties of resin-matrix ceramics.

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Chinese Journal of Tissue Engineering Research•2026

Immunological mechanisms of Xuling Jiangu Formula in intervening osteoporosis model rats

Authors: Huang Jingwen, Li Shengqiang, Jiang Hong, Chen Xuan, Ye Yunjin, Ge Jirong

BACKGROUND: Osteoporosis is not only a metabolic disease, but also an inflammatory or autoimmune disease. Immune cells Treg and Th17 have a mutually antagonistic effect on the differentiation and maturation of osteoclasts, and the maintenance of cell balance between the two is the basis for ensuring normal bone metabolism. OBJECTIVE: To explore the immunomodulatory mechanism of Xuling Jiangu Formula on osteoporosis and its relationship with the balance of Treg/Th17 cells. METHODS: Sprague-Dawley rats were randomly divided into a sham operation group, a model group, and a drug group, with eight rats in each group. The latter two groups underwent bilateral ovariectomy to establish the animal model; the sham operation group underwent the same procedure except for ovary removal. Four weeks after modeling, bone mineral density was measured using dual-energy X-ray absorptiometry to evaluate whether the modeling was successful. Drug intervention started 4 weeks after surgery: the Xuling Jiangu Formula group was given 10 mL/kg Xuling Jiangu Formula by gavage once daily for 16 weeks; the model and sham operation groups were given the same volume of normal saline. After 16 weeks of drug administration, bone mineral density and blood routine parameters were measured, bone tissue morphology was observed by hematoxylin-eosin staining, serum immune factor levels were detected by ELISA, and the gene and protein expressions of osteoprotegerin, receptor activator of nuclear factor-κB ligand, retinoic acid-related orphan receptor γt, and forkhead box P3 were detected by quantitative PCR and western blot. The numbers of Treg and Th17 cells were detected by flow cytometry. RESULTS AND CONCLUSION: After 16 weeks of administration, compared with the model group, the bone mineral density of rats in the Xuling Jiangu Formula group was significantly increased (P < 0.05), serum levels of interleukin-10 and transforming growth factor-β were increased but without significant difference, while levels of interleukin-17 and interleukin-6 were significantly decreased (P < 0.05). After 16 weeks of administration, the gene and protein expressions of osteoprotegerin and Treg marker gene forkhead box P3 were significantly increased (P < 0.05), while the gene and protein expressions of Th17 marker gene retinoic acid-related orphan receptor γt were significantly decreased (P < 0.05), and the protein expression of receptor activator of nuclear factor-κB ligand was significantly decreased (P < 0.05), but the gene expression showed a decreasing trend without significant difference. Flow cytometry results showed that the number of Treg cells was significantly increased (P < 0.05), while the number of Th17 cells was decreased but not statistically significant. These findings suggest that the immune mechanism of Xuling Jiangu Formula in treating osteoporosis is to affect the Treg/Th17 balance by increasing the number of Treg cells, then reduce the secretion of interleukin-17 and interleukin-6, promote the upregulation of forkhead box P3 and downregulation of retinoic acid-related orphan receptor γt, thereby changing the osteoprotegerin/receptor activator of nuclear factor-κB ligand ratio, and subsequently inhibit osteoclast differentiation.

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Chinese Journal of Tissue Engineering Research•2026

Application of tissue clearing technology in a rat model of chronic spinal cord injury

Authors: WANG Zhizhuang, XU Bo, MA Guoliang, ZHANG Dan, QIN Xiaokuan, FENG Minshan, CHEN Xin, YANG Kexin, YANG Bowen, YIN He

BACKGROUND: Studies have shown that tissue clearing technology enables the three-dimensional (3D) visualization of neurons in the spinal cord injury area, clearly presenting morphological changes of neurons, including soma atrophy, dendrite fragmentation, and axonal degeneration. OBJECTIVE: To systematically evaluate the application potential of tissue clearing technology in a rat model of chronic spinal cord injury. METHODS: Thirty-six female Sprague-Dawley rats were randomly and equally divided into a normal group (n=12), a sham surgery group (n=12), and a surgery group (n=12). The normal group received no treatment. The sham group underwent implantation and immediate removal of a poly(vinyl alcohol)/polyacrylamide interpenetrating network hydrogel into the C5-C7 spinal canal. The surgery group received implantation of the hydrogel to compress the spinal cord at C5-C7 to establish a chronic spinal cord injury model. At postoperative days 1, 3, 7, and 14, motor function was assessed using the Basso, Beattie, and Bresnahan (BBB) score and the modified Rivlin inclined plane test. At day 14, spinal cord tissue was harvested for hematoxylin-eosin staining to observe morphology, and tissue clearing combined with neuron-specific nuclear protein immunofluorescence labeling was used for three-dimensional reconstruction and cross-sectional view analysis. RESULTS AND CONCLUSION: (1) The BBB scores and inclined plane test angles in the surgery group were significantly lower than those in the normal and sham groups at all time points (P < 0.001). (2) Hematoxylin-eosin staining showed significant spinal cord injury in the surgery group, with swelling and destruction of nerve cells in the gray matter, loss of uniformity in white matter structure, disappearance of some nuclei, reduced cell number, massive glial cell proliferation and aggregation in the compression area, disordered white matter structure, and formation of numerous cavities. (3) Three-dimensional reconstruction and cross-sectional analysis of the spinal cord showed that in the normal and sham groups, the spinal cord appeared continuous and full, with uniform distribution of neuron-specific nuclear protein red fluorescence, dense layered arrangement of neurons in the anterior horn of the gray matter, and intact white matter fiber tracts. In the surgery group, the spinal cord appeared depressed or even interrupted, with significantly reduced fluorescence intensity of neuron-specific nuclear protein in the compressed segment, disrupted gray matter neuronal layer structure, and regional fluorescence interruption. These results indicate that tissue clearing technology can effectively display structural changes after spinal cord injury, providing strong support for studying the pathological mechanisms of spinal cord injury.

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Chinese Journal of Tissue Engineering Research•2026

Transcriptomic analysis of expression and function of differential genes in traditional Chinese medicine syndromes of postmenopausal osteoporosis

Authors: HE Yanyan, GE Jirong, LI Shengqiang, CHEN Xuan, HUANG Jingwen, HUANG Xiaobin, XUE Lipeng

BACKGROUND: Kidney yin-yang deficiency syndrome in postmenopausal osteoporosis holds particular clinical significance due to its complex features of yin-yang imbalance, and analysis of its differential genes is key to revealing molecular mechanisms. OBJECTIVE: To compare differential gene expression profiles among different kidney deficiency syndromes of postmenopausal osteoporosis, screen for differential genes and signaling pathways associated with kidney yin-yang deficiency syndrome, reveal its molecular biological characteristics, and provide a basis for the objectification of traditional Chinese medicine syndromes. METHODS: Eighteen postmenopausal osteoporosis patients with kidney deficiency syndromes (kidney yang deficiency, kidney yin deficiency, and kidney yin-yang deficiency, 6 cases each) were included, and 6 healthy postmenopausal women served as healthy controls. Transcriptome sequencing was used to screen differential genes, followed by Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses. The expression levels of four target genes (HSP90AB4P, CTU1, ST6GALNAC2, PTGS2) were validated by qRT-PCR. RESULTS AND CONCLUSION: (1) Compared with healthy controls, kidney yin deficiency, and kidney yang deficiency groups, the kidney yin-yang deficiency group had 235, 247, and 4,557 differentially expressed genes, respectively. Intersection analysis of the three comparison groups identified 22 differential genes associated with kidney yin-yang deficiency syndrome (18 up-regulated, 4 down-regulated). (2) qRT-PCR validation showed that the up/down regulation trends of target genes were consistent with transcriptome sequencing results. (3) Gene Ontology analysis showed that biological processes focused on energy metabolism (NAD synthesis and metabolism) and physiological homeostasis (thermogenesis, blood pressure regulation), molecular functions involved immune defense, metabolic regulation, inflammation and signal transduction, ion channel regulation, etc.; cellular components were related to ribosomes, endoplasmic reticulum, nucleus, and tRNA modification. (4) Kyoto Encyclopedia of Genes and Genomes enrichment identified 60 pathways, including apoptotic cell clearance, nuclear factor kappa B, tumor necrosis factor, interleukin-17, vascular endothelial growth factor, forkhead box O signaling pathways, and metabolic pathways. (5) These findings suggest that postmenopausal osteoporosis with kidney yin-yang deficiency syndrome is a comprehensive manifestation of multidimensional molecular network imbalance, related to ribosomal synthesis disorders, non-coding RNA and signal transduction and transcriptional regulation, immune-inflammatory regulation, and metabolic transport.

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Chinese Journal of Tissue Engineering Research•2026

Highly sensitive indicators of neck muscle fatigue derived from multimodal electrophysiological and metabolic coupling analysis

Authors: LIU Ya-kun, LU Guang-qi, LIANG Long, LI Jing, SUN Xin-yue, LIU Guang-wei, ZHOU Shuai-qi, MAO Han-ze, MA Ming-ming, HU Jia-ming, ZHU Li-guo, ZHUANG Ming-hui, YU Jie

BACKGROUND: Prolonged forward head posture induces neck muscle fatigue, a significant contributing factor to cervical spondylosis. Current unimodal monitoring approaches are inadequate to capture the dynamic coupling among muscle activation, metabolic activity, and motor control. OBJECTIVE: To systematically evaluate the temporal characteristics of neck muscle fatigue using multimodal monitoring technology, thereby providing a theoretical foundation for early detection and intervention of cervical fatigue. METHODS: Twenty healthy participants were recruited. Surface electromyography, near-infrared spectroscopy, and three-dimensional motion capture technology were synchronized to record electrophysiological signals, oxygenated hemoglobin concentration, and cervical kinematics during a sustained 45° static forward flexion task until subjective fatigue was reached (Borg CR-10 score ≥ 4). Temporal changes in root mean square amplitude, mean power frequency, muscle oxygen saturation, and normalized forward head angle were analyzed across fatigue stages segmented into 10% intervals of total endurance time. RESULTS AND CONCLUSION: (1) The root mean square amplitude increased significantly (P < 0.001), while mean power frequency and muscle oxygen saturation decreased significantly (P < 0.001) throughout the task, with the reduction in muscle oxygen saturation commencing from the 40% fatigue stage. (2) Linear regression analysis between mean power frequency and muscle oxygen saturation showed high explanatory power (upper trapezius R²=0.58, middle trapezius R²=0.61), and metabolic compensation preceded significant electrophysiological changes. (3) The upper trapezius entered fatigue earlier than the middle trapezius (P < 0.05). These results indicate that combined monitoring of mean power frequency and muscle oxygen saturation provides highly sensitive indicators for early warning of neck muscle fatigue.

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Stem Cell Research & Therapy•2026

iPSC-derived exosomes promote diabetic wound healing by attenuating inflammatory responses

Authors: Li Long, Ju Qiao, Liang Wang, Yue Wang, Yi Xu, Hui Chen, Hongzhong Jin, Wei He, Xiaohong Han, Jianmin Zhang

Background: Owing to impaired glucose metabolism, the high-glucose microenvironment in diabetic patients disrupts a series of biological reactions that hinder the wound healing process, resulting in a significant cost to the health care system and an urgent need for new and advanced therapies. Methods: In this study, induced pluripotent stem cell-derived exosomes (iPSC-Exos) were isolated from iPSC culture supernatant via centrifugation and ultrafiltration. We evaluated the therapeutic effects of iPSC-Exos on diabetic wound healing through two clinically relevant animal models (spontaneous genetic diabetic mouse model and streptozotocin (STZ)-induced diabetic mouse model). iPSC-Exos were topically administered to full-thickness cutaneous wounds in diabetic mice. The therapeutic effects were systematically assessed by measuring wound closure rates, conducting comprehensive histopathological evaluations, and performing quantitative analysis of inflammatory mediators via ELISA. Results: We demonstrated that iPSC-Exos can significantly accelerate diabetic wound healing through two clinically relevant animal models (spontaneous genetic diabetic mouse model and STZ-induced diabetic mouse model) for the first time. The multifaceted therapeutic mechanisms include: (i) Direct activation of tissue regeneration (promotion of re-epithelialization, tissue remodeling and scar attenuation); (ii) Modulation of the inflammatory microenvironment (promoting macrophage polarization toward anti-inflammatory M2 phenotype/suppressing inflammation). Conclusions: This dual-animal model approach, which closely recapitulates key pathophysiological features of human diabetic wounds, offers superior clinical translatability compared to single-animal model studies. Our findings iPSC-derived exosomes promote diabetic wound healing by attenuating inflammatory responses.

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Stem Cell Research & Therapy•2026

Stem cell-based therapies for alopecia areata: a narrative review

Authors: Aiping Fan, Mingjuan Liu, Jun Li

Alopecia Areata (AA) is a chronic inflammatory disorder characterized by non-scarring, patchy hair loss that may progress to the entire scalp (alopecia totalis) or body (alopecia universalis), significantly impairing patients’ quality of life and psychological health. Although the exact pathogenesis of AA remains unclear, current evidence suggests that the breakdown of hair follicle immune privilege (IP) and subsequent autoimmune-mediated follicular attack play a pivotal role. Conventional therapeutic modalities, including corticosteroid and Janus kinase (JAK) inhibitors, are often limited by suboptimal efficacy in severe cases and high relapse rates following treatment cessation. In recent years, stem cell-based therapy has emerged as a novel treatment for AA, showing therapeutic potential through multiple mechanisms. Preliminary clinical trials have indicated significant efficacy in promoting hair regrowth among AA patients. However, comprehensive evaluation of long-term safety and therapeutic efficacy remains imperative. This review article aims to give a comprehensive overview of the recent advances in stem cell-based therapies for AA and explore their underlying mechanisms and clinical application prospects, hoping to provide a framework and reference for future research and clinical practice.

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Stem Cell Research & Therapy•2026

Research based on serine metabolism indicates mesenchymal stem cells alleviate psoriasis by regulating the PSPH-PINK1-Parkin-NLRP3 pathway in HaCaT

Authors: Qing Lin, Yunfei Ji, Bin Yang, Rongjia Zhu, Ping Song, Robert chunhua Zhao

Background Psoriasis is a refractory immune-related disease. In recent years, it has been discovered that mesenchymal stem cells (MSCs) can be used as a new therapeutic approach for psoriasis, but their potential therapeutic mechanism remains unclear. This study aims to explore the role of MSCs in the treatment of psoriasis. Methods We employed a mouse psoriasis model induced by imiquimod (IMQ) in vivo and a co-culture system of MSCs and HaCaT keratinocytes (KCs) cell line in vitro. These approaches allowed us to investigate the effect of MSCs on the levels of inflammatory factors and the activation of inflammasomes in both contexts. Mouse-targeted amino acid sequencing, transmission electron microscopy for in vitro observation, immunofluorescence for both in vivo and in vitro analyses, and siRNA transfection in vitro were employed in this study. Results Our results showed that MSCs significantly improved the skin lesion of mice with psoriasis, and reduced the levels of inflammatory factors and chemokines including IL-1β, IL-6, IL-8, TNF-α, MCP-1, CCL7, CCL20 and CCL27 in the mouse skin lesion areas and M5- induced psoriatic KCs models in vitro. Likewise, MSCs repaired the skin barrier by enhancing claudin-1 expression in vivo. In addition, MSCs increased KRT1 and decreased KRT6 levels in vivo and in vitro. Amino acid metabolism analysis showed that MSCs could improve the serine metabolism level in the mouse skins and upregulated the key enzyme phosphoserine phosphatase (PSPH) in serine metabolism. In vitro experiments demonstrated that knockdown of PSPH could reverse the therapeutic effects of MSCs on psoriasis. Furthermore, studies in vitro and in vivo revealed that MSCs can activate the PINK1-Parkin pathway. It was specifically manifested by elevated levels of PINK1, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, coupled with a reduction in P62 protein. Subsequently, the activation of PINK1-Parkin led to decreased expressions of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1. In vitro and in vivo experiments indicated that MSCs can reduce the levels of IL-1β, IL-6, IL-8, TNF-α, CCL7, CCL20, CCL27, and MCP-1 by inhibiting the activation of NLRP3 inflammasomes. Meanwhile, PSPH knockdown in vitro can reverse the activating effects of MSCs on the PINK1-Parkin, as shown by decreased levels of PINK, Parkin, p-Parkin, Beclin-1, and LC3B-II/I, concurrently with an elevation in P62. Conclusions The results of this study indicated that MSCs can alleviate IMQ-induced psoriasiform dermatitis in mice by upregulating serine metabolism. The key serine metabolism enzyme PSPH may enhance PINK1/Parkin-mediated mitochondrial autophagy in psoriatic HaCaT and inhibit NLRP3 inflammasome activation in HaCaT cells, thereby alleviating skin inflammatory responses and suppressing skin proliferation in psoriatic mice.

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Stem Cell Research & Therapy•2026

Spatiotemporal single-cell atlas of suture stem cell dynamics in craniosynostosis

Authors: Xinyan Chen, Chenzhi Lai, Tian He, Zong Chen, Xiaolei Jin

Background: Craniosynostosis is a congenital disorder characterized by premature suture fusion and aberrant skull morphogenesis. The cellular dynamics and regulatory mechanisms of suture mesenchymal stem cells (SuSCs) in this disease remain poorly defined. Methods: We integrated single-cell RNA sequencing and 2-μm-resolution Visium HD spatial transcriptomics to build a spatiotemporal atlas of coronal suture cells in Fgfr2C342Y/+ mice, a murine model recapitulating human Crouzon syndrome, alongside wild-type controls across three key developmental stages (E14.5, E18.5, and P3). To obtain near single-cell spatial resolution, we created SpatialCell, which combines morphology-based segmentation and machine-learning classification using a reference trained on our single-cell datasets. Results: The atlas reveals stage-specific remodeling of SuSC niches and a shift of SuSC spatial associations toward osteogenic mesenchyme in craniosynostosis. Along the SuSC-to-osteoblast trajectory, pre-osteoblasts were depleted earlier than upstream SuSCs, and SuSCs displayed premature acquisition of osteogenic programs near the suture midline. Temporal Gene Ontology patterns indicated early extracellular-matrix disruption, mid-gestation chondrogenic activation, and postnatal mineralization. Network analysis nominated Foxa3 as a candidate regulator in SuSC subsets; siRNA knockdown of Foxa3 reduced ex vivo mineralization in the craniosynostosis background. Spatial communication analyses implicated signals from suture meningeal fibroblasts and immune cells that converge on SuSC fate. Conclusions: Our results support a model where craniosynostosis may involve disrupted temporal coordination of developmental programs, not merely accelerated bone formation. The atlas and analytic framework pinpoint when and where SuSC fate diverges, propose Foxa3 as an intervention target, and provide a high-resolution resource for mechanistic and therapeutic exploration.

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Acta Biochimica et Biophysica Sinica•2026

Distinct miR319a identified from Persicaria chinensis mediates cross-kingdom suppression of cervical cancer by targeting ITGA3

Authors: Yueyue Yan, Dan Bai, Lei Li, Leimei Xu, Hua Yang, Yuhui Wang, Han Feng, Lan Zhu

Persicaria chinensis, a well-known traditional Chinese medicinal herb that is both edible and medicinal, has been widely acknowledged for its therapeutic effects, such as anti-inflammatory, antioxidant, and antitumor activities. However, the role of miRNAs from this plant in the cross-kingdom regulation of human diseases has not been investigated. In this study, we analyze the miRNA expression profile of P. chinensis using high-throughput sequencing and identify a total of 673 miRNAs, including 422 novel miRNAs that are unique to this plant and 251 conserved miRNAs. Among the conserved miRNAs, pch-miR319a is found to be the most abundant. Moreover, food-oriented pch-miR319a accumulates in the uterus and tumors and exhibits a rich repertoire of target genes within cancer-related pathways, demonstrating significant cross-kingdom regulatory potential. Utilizing the dual-luciferase reporter gene assay, we demonstrate that pch-miR319a from P. chinensis targets the Itga3 gene, which is associated with cervical cancer progression. Overexpression of pch-miR319a significantly decreases the viability, migration, and induces apoptosis of HeLa cervical cancer cells in vitro. Moreover, in a syngeneic mouse tumor model of cervical cancer, treatment with pch-miR319a effectively inhibits tumor growth and downregulates the expressions of ITGA3 and the proliferation marker Ki-67. Our study highlights the potential of pch-miR319a from P. chinensis as a novel therapeutic agent for cervical cancer by targeting ITGA3 and provides new insights into the cross-kingdom regulatory mechanisms of plant miRNAs in human diseases.

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Acta Biochimica et Biophysica Sinica•2026

Biochemical and structural studies reveal the substrate specificity and catalytic mechanism of MYG1 as a two-metal ion-dependent 3′→5′ exonuclease

Authors: Chao Lan, Ziyue Chen, Guanchao Wang, Jianping Ding

Nucleases are a class of enzymes that specifically cleave nucleic acids in all living organisms. They play crucial roles in essential biological processes, including the regulation of gene expression, DNA damage repair, and RNA processing and degradation. MYG1 (melanocyte proliferating gene 1) is a highly conserved eukaryotic protein that exhibits 3′→5′ exonuclease activity. This study systematically characterizes the enzymatic properties of MYG1 and determines its structures in complexes with metal ions and various mono- and poly-(deoxy)nucleotides. The functional roles of key residues involved in metal ion binding and substrate binding in the catalytic reaction are examined through site-directed mutagenesis, enzymatic activity assay, and structure determination. Our biochemical and structural data together demonstrate that MYG1 is a Mn2+- or Mg2+-dependent 3′→5′ exonuclease capable of cleaving a variety of nucleic acids with different structures. It exhibits the highest activity for single-stranded RNA and a nucleotide preference for U in single-stranded RNA and dT in single-stranded DNA. Mechanistically, MYG1 functions as a dimer, with the active site formed by the catalytic domain of monomer 1 and the substrate-binding domain of monomer 2, and cleaves nucleic acids through a two-metal ion-mediated catalytic mechanism. These findings establish a molecular basis for further investigations into the biological functions and molecular mechanisms of MYG1 within cells and its potential roles in human diseases.

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Acta Biochimica et Biophysica Sinica•2026

Biochemical and structural studies of the midnolin Catch domain bound with both wild-type and mutant IRF4 peptides reveal the molecular basis for its broad substrate specificity

Authors: Yanling Zhong, Ziyue Chen, Guanchao Wang, Jianping Ding

The newly discovered midnolin-proteasome pathway is a unique ubiquitin-independent mechanism for degrading nuclear proteins, which is crucial for maintaining cellular protein homeostasis. The Catch domain of midnolin is essential for substrate recognition and binding, yet the underlying mechanism for its broad substrate specificity remains elusive. Transcription factor IRF4, essential for the functions of B and T cells, is a substrate of midnolin. This study presents comprehensive biochemical and structural analyses of the human midnolin Catch domain in complexes with both wild-type and mutant IRF4 peptides. The crystal structure of the Catch-IRF4 complex reveals that the Catch domain creates a substrate-binding groove at the interface of the Catch1 and Catch2 subdomains, recognizing and binding to the 215-QVTGTFYAC-223 sequence motif of IRF4. The binding motif of IRF4 forms a β-strand that is embedded into the substrate-binding groove, resulting in an antiparallel five-stranded β-sheet. The interactions between the IRF4 peptide and the Catch domain are predominantly hydrophobic and exhibit high spatial complementarity. Additionally, the biochemical, modeling and structural data indicate that the V2 and A8 positions of the IRF4 sequence motif can be substituted with other hydrophobic or small polar residues (G/A/V/L/I/M/P/F/Y/C/S/T), but not with large polar and charged residues (D/N/E/Q/H/K/R). The G4 position can be replaced by Ser, while the F6 position can be substituted with Tyr. These results suggest that the Catch domain can recognize and bind to a variety of substrates containing the sequence motif x[G/A/V/L/I/M/P/F/Y/C/S/T]x[G/S]x[F/Y]x[G/A/V/L/I/M/P/F/Y/C/S/T]x or briefly the G/SxF/Y motif (where x represents polar residues) located in an unstructured or loop region on the protein surface, and the hydrophobic interactions and spatial complementarity between the binding motifs of substrates and the Catch domain govern the substrate specificity. Collectively, these findings elucidate the molecular basis for midnolin’s broad substrate specificity.

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Acta Biochimica et Biophysica Sinica•2026

RNF126 writes a non-canonical ubiquitin code on midnolin to tune protein stability

Authors: Yun Yang, Jin Ren, Xiang Qiu, Yanlin Liu, Shilin Yuan, Ronggui Hu, Zhixiong Xia, Chuanyin Li

Midnolin (MIDN) is a newly recognized master regulator that drives ubiquitin-independent proteasomal degradation, yet the mechanisms governing its own turnover remain enigmatic. Here, we demonstrate that MIDN is ubiquitinated and identify RNF126 as the cognate E3 ligase. RNF126 physically associates with MIDN and catalyzes its ubiquitination, and mass spectrometry mapping reveals that this process occurs primarily at non-canonical cysteine, serine, and threonine residues (C230, C236, S237, T239, and S241) rather than at lysine residues. This non-classical ubiquitination targets MIDN for 26S-proteasomal degradation. In vivo dissection of the RNF126-MIDN axis shows that it governs EGR1 abundance and, consequently, the tumor-suppressor proteins PTEN and p53, thereby restraining the progression of testicular germ-cell tumors (TGCTs). Our findings reveal an unappreciated layer of MIDN regulation and identify the RNF126-MIDN ubiquitination cascade as a potential therapeutic vulnerability in TGCTs and related malignancies.

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Acta Biochimica et Biophysica Sinica•2026

cGAS-STING pathway reprograms macrophage polarization and is highly expressed in responding tumors after neoadjuvant immunotherapy in head and neck carcinoma

Authors: Zhaohong An, Xiwei Zhang, Lin Li, Dilinaer Wusiman, Zhaoyang Wang, Fa Zhang, Xiaohui Zhao, Changming An, Zhenzhen Yin, Wei Gao

Given the critical role of the cGAS-STING pathway in antitumor immunity, this study investigates the functional role of STING in head and neck squamous cell carcinoma (HNSCC) to evaluate the therapeutic potential of STING agonists. Analysis of the TCGA-HNSC dataset reveals that elevated expression of the STING-encoding gene TMEM173 is significantly correlated with increased M1 macrophage infiltration and enrichment of macrophage polarization-related signaling pathways. In vitro experiments in which RAW 264.7 cells are co-cultured with tumor cell-conditioned medium demonstrate that the STING agonist MSA-2 effectively reprograms tumor-induced M2-polarized macrophages toward the M1 phenotype. This MSA-2-induced M1 polarization is accompanied by increased expressions of IFN-α, IFN-β, IFN-γ, TNF-α, and IL-6, while the STING inhibitor H-151 reverses these effects. Flow cytometry further reveals that MSA-2 treatment reduces PD-1 and increases MHC II expression on macrophages. Immunohistochemical analysis of clinical samples confirms that high STING expression is correlated with increased numbers of CD68⁺ and CD80⁺ (M1-like) macrophages. In support of translational relevance, analysis of single-cell RNA-seq data from HNSCC patients receiving neoadjuvant immunotherapy indicates that TMEM173 is expressed primarily in T cells and macrophages and that the cGAS-STING pathway score is significantly higher in patients who respond to treatment. Collectively, these findings provide systematic clinical and experimental evidence supporting the potential of STING agonists, such as MSA-2, to enhance antitumor immunity in HNSCC, particularly when combined with immunotherapy.

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Acta Biochimica et Biophysica Sinica•2026

Serum starvation induces density-dependent apoptosis via HIF-1 activation and JNK suppression

Authors: Qifan Yang, Yaofeng Hu, Jiahui Lv, Jiaqi Xue, Jiaqi Chen, Changwan Wang, Fajian Hou

Serum deprivation is a well-established inducer of apoptosis, yet the molecular mechanisms governing this process remain incompletely understood. Here, we show that serum starvation selectively triggers intrinsic apoptosis in high-density murine embryonic fibroblasts (MEFs) through coordinated HIF-1α activation and JNK signaling suppression. Knockdown of HIF-1α abolishes caspase-3 activation and apoptosis induced by serum deprivation, whereas upregulation of HIF-1α in low-density cells recapitulates the apoptotic response observed in high-density cultures. Simultaneously, serum deprivation leads to the suppression of the JNK pathway, which contributes to apoptosis. Notably, combined HIF-1α activation and JNK inhibition in low-density cells fully mimics the apoptotic phenotype of high-density conditions, underscoring the interplay between these pathways. Together, these findings define a density-dependent apoptotic switch in which HIF-1α drives metabolic stress adaptation, whereas JNK suppression removes a critical survival signal, converging to promote mitochondrial-mediated cell death. This work provides a mechanistic framework for understanding nutrient stress-induced apoptosis and suggests potential therapeutic targets for diseases characterized by aberrant cell survival.

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Acta Biochimica et Biophysica Sinica•2026

Celastrol alleviates SGLT2 inhibitor-induced diabetic hyperketonemia by inhibiting hepatic ketogenesis

Authors: ZHU Yinghan, WANG Yiting, ZHANG Minglong, LIU Lingxu, TIAN Yang, GUO Zeyu, ZHANG Ran, ZHANG Jinrui, MA Zhenyu, FANG Fude, YAN Li, LIU Xiaojun

SGLT2 inhibitor (SGLT2i)-induced diabetic hyperketonemia is a life-threatening acute complication of diabetes. While celastrol has been reported to have beneficial effects on obesity, its potential role in ketogenesis remains unclear. In this study, celastrol administration significantly attenuates the fasting-induced increase in blood β-hydroxybutyrate levels. Moreover, a 7-day course of celastrol (1 mg/kg/day) leads to reductions in body weight and fat mass. Mechanistically, celastrol specifically downregulates HMGCS2 expression and suppresses hepatic ketogenesis through the inhibition of PPARα expression in the short term (≤ 2 days). However, after prolonged treatment for 7 days, celastrol modulates both PPARα and serum free fatty acid (FFA) levels. Furthermore, the anti-ketogenic effect of celastrol is abolished in Pparα⁻/⁻ mice. Importantly, celastrol effectively ameliorates SGLT2i-induced hyperketonemia. In summary, celastrol curbs hepatic ketone overproduction in a PPARα-dependent manner, indicating its protective potential against SGLT2i-induced hyperketonemia.

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Acta Biochimica et Biophysica Sinica•2026

Yaf9 conditionally contributes to cell size control in Candida albicans

Authors: Wencheng Zhu, Baodi Dai, Yinxing Xu, Jiangye Chen

Candida albicans is an opportunistic fungal pathogen renowned for its ability to transition between distinct phenotypic states, such as the yeast-hyphae transition and the white-opaque switching. This morphological plasticity allows the organism to adapt to various host environments and evade immune responses. The white state is characterized by yeast-like cells with high proliferative capacity, whereas the opaque state features elongated cells with enhanced mating ability. The regulation of white-opaque switching is primarily controlled by a complex network of transcription factors. White-Opaque Regulator 1 (Wor1) serves as a master regulator crucial for the establishment and maintenance of the opaque state by activating the expression of genes required for opaque cell formation [1–3]. Conversely, the Mating-Type Like (MTL) locus in C. albicans acts as a critical barrier to white-opaque switching. The genes present at this locus strictly repress the white-to-opaque transition by the formation of a1/α2 complex; therefore, only MTLa/a or MTLα/α strains frequently switch to the opaque state [4,5]. Although the MTLa/α lab strain CAI4 is typically locked in the white state, some MTLa/α clinical isolates can switch to opaque [6]. Several genes were found to modulate this repression. For example, loss of HBR1, which is an activator of MTLALPHA1 and MTLALPHA2 gene expression, enables switching in MTLa/α cells [7]. Deletion of transcriptional repressors of the opaque state such as TUP1 also facilitates white-to-opaque switching [8]. The SWR1 complex incorporates H2A.Z into chromatin, and loss of Swr1 enhances switching and stabilizes the opaque state in MTL homozygous cells [9]. Our previous work revealed that the NuA4 histone acetyltransferase complex and the SWR1 complex merge into a supercomplex via Yaf9 in white-state yeast cells in C. albicans [10]. Here, we first tested whether Yaf9 is involved in white-to-opaque switching in MTLa/α heterozygous cells. The knockout of the YAF9 gene was validated by genotyping and qRT-PCR, confirming its loss at both the genomic and transcriptional levels (Supplementary Figure S1). The yaf9 null mutant cells were spread onto YPD plates and incubated in 20% CO2 at 25°C. After eight days of growth, sectors containing opaque cells were observed (Figure 1A). The frequency of opaque cell formation in the yaf9 mutant exceeded that in wild-type (WT) cells overexpressing WOR1 (Figure 1B). qRT-PCR analysis confirmed significant upregulation of opaque cell-specific markers, including WOR1 and OP4, in yaf9 mutant opaque cells, whereas the white cell marker WH11 was downregulated (Figure 1C). To examine whether YAF9 deletion affects the expression of MTL genes, we performed qRT-PCR for MTLA1 and MTLALPHA2 in white WT cells and in both white and opaque yaf9 mutant cells. The expression of both genes remained unchanged in yaf9 mutant cells (Figure 1D), suggesting that Yaf9-mediated repression of white-to-opaque switching occurs independently of MTL gene regulation. As Yaf9 is a component of the NuA4 and SWR1 complexes, we next investigated the roles of the NuA4 core enzyme Esa1 and the SWR1 core enzyme Swr1 in white-to-opaque switching in MTLa/α heterozygous cells. As shown in Figure 1E (upper panel), esa1 cells failed to switch to the opaque form under 20% CO2 stimulation, indicating that Esa1 activity is essential for opaque cell formation under the tested conditions. In contrast, swr1 cells readily underwent white-to-opaque switching (Figure 1E, lower panel), similar to the yaf9 mutant. These results indicate that Yaf9 functions as a repressor of white-to-opaque switching and that its deletion bypasses the repression imposed by the MTLa/α configuration. We then examined the role of YAF9 in white-to-opaque switching in MTLa/a cells, where MTL repression is removed. In air, yaf9 cells remained white; however, when exposed to 20% CO2, they frequently (> 50%) switched to the opaque form, which occurred at a significantly higher frequency than WT cells (Figure 2A,B). Notably, yaf9 cells exhibited a novel elongated opaque morphology, which we term e-Op cells. Quantification revealed that e-Op cells had similar width but were two to three times longer than WT opaque cells (Figure 2C). At the transcriptional level, e-Op cells displayed comparable upregulation of WOR1 and OP4 and downregulation of WH11 (Figure 2D). Notably, WH11 expression in yaf9 white cells was slightly higher than that in WT white cells. Like white cells, opaque cells are also capable of forming filaments under specific conditions [11]. To determine whether e-Op cells represent a filamentous form of opaque cells, we examined their gene expression and morphological stability. Multiple lines of evidence indicate that e-Op cells are distinct from these filamentous forms. First, when cultured on SOR medium, which promotes filamentous g

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Acta Biochimica et Biophysica Sinica•2026

Explore antibody repertoire in the era of AI

Authors: Yudi Zhang, Hefei Wang, Chencheng Liu, Fei-Long Meng

The diverse antibodies of adaptive immunity comprise an antibody repertoire that combats various pathogens. This repertoire is shaped by both intrinsic antibody gene diversification and extrinsic cellular selection. Conversely, an antibody repertoire contains multiple layers of immunological information, including the history of pathogen exposure. High-throughput sequencing-based antibody repertoire cloning approaches have revealed unexpected features of adaptive immunity. However, our understanding of antibody repertoire data is still in its infancy. In this review, we introduce the emerging concepts and discuss the application of deep learning approaches to understanding antibody repertoires. First, we introduce the definition and functional features of antibody clonotype. Next, we review the evolution of antibody clonotypes and discuss potential antibody repertoire-directed vaccination approaches. Lastly, we summarize the application of deep learning in predicting antibody binding, generating specific antibodies, and making immunologic diagnoses. Recently, artificial intelligence (AI) has made revolutionary progress in biology. Leveraging high-dimensional antibody repertoire information, deep learning models have the potential to transform our understanding of antibody repertoire.

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Acta Biochimica et Biophysica Sinica•2026

The dual role of whole-genome duplication: biological mechanisms, functional consequences, and detection advances

Authors: Yawei Song, Jiajie Yang, Shuheng Wu, Wei Wu

Whole-genome duplication (WGD) represents an evolutionarily conserved process occurring in prokaryotes, eukaryotes, and somatic mammalian tissues. While developmentally programmed WGD supports normal tissue regeneration, unscheduled WGD drives chromosomal instability and oncogenic progression in cancer. Recent studies have clarified dual roles of WGD across physiological homeostasis and disease pathogenesis. Here, we review the prevalence of WGD, the molecular mechanisms driving its major causes and its biological consequences. In addition, we highlight recent advancements in WGD detection, including both conventional cytogenetic techniques and newly developed high-throughput sequencing approaches. The integration of multi-omics and machine learning further improves ploidy analysis, particularly in cancer research. Together, these insights establish WGD as a critical regulator of development, regeneration, and disease and underscore the importance of emerging computational and sequencing tools for its precise characterization.

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Acta Biochimica et Biophysica Sinica•2026

Special issue: advances in immunology and its applications

Authors: Mingshun Han, Hongyan Wang

Innate immunity and adaptive immunity play crucial roles in regulating inflammation-related diseases such as tumors, infections, and autoimmune diseases. The interplay between innate immunity and adaptive immunity ensures the maintenance of tissue homeostasis and effective clearance of invading pathogens or tumor cells. However, dysregulation in each type of immune cells or their communications leads to pathological conditions, ranging from chronic inflammation to malignant progression. In recent years, the field of immunology has witnessed a paradigm shift, moving from merely describing immune cell signaling or phenotypes to actively exploring strategies that reshape immune functions for therapeutic benefit. Exploring effectors or strategies to reshape T cell function for the improved anti-tumor and anti-infection efficacy has emerged as a critical research direction. This includes the development and optimization of chimeric antigen receptor T-cell (CAR-T) therapies for clinical applications. While CAR-T therapy has revolutionized the treatment of hematologic malignancies, its success in solid tumors remains limited. Chen et al. [1] dissect the distinct signaling mechanisms of chimeric antigen receptors (CARs) compared to T cell receptors (TCRs). They elucidate how CAR-T cells, despite overcoming MHC restrictions, encounter significant hurdles such as inefficient tumor infiltration and the hostility of the immunosuppressive tumor microenvironment (TME). To address these challenges, the authors underscore several innovative strategies, such as optimizing receptor clustering to facilitate immune synapse formation and integrating novel co-stimulatory domains to augment therapeutic efficacy in solid tumors. Moving beyond engineering, fundamental insights into microenvironmental stress and T cell intrinsic signaling are pivotal. While oxidative stress is a well-established concept in the TME, Ji and Xiao [2] draw attention to the phenomenon of “reductive stress”. They explain how a surplus of intracellular reducing agents disrupts redox balance, creating a reductive environment that significantly influences immune cell differentiation and tumor survival. In a complementary study, Shi et al. [3] investigate the intrinsic role of pattern recognition receptor (PRR) signaling within T cells. Although PRRs are historically classified as innate sensors, this review highlights their critical function in adaptive immunity, discussing how T cells utilize PRRs to interpret endogenous danger signals and microbial cues to regulate cytokine release and proliferation. Additionally, Ma et al. [4] provide a comprehensive update on T cell immunoglobulin and mucin-containing molecule 3 (TIM-3), an important immune checkpoint. By detailing its expression profile across T cells, NK cells, and myeloid lineages, they propose that rational combination therapies targeting TIM-3 alongside other checkpoints offer a promising avenue to surmount current resistance mechanisms. This issue also highlights the regulation of immunity by neurotransmitters and biological rhythms, illustrating the profound integration of the immune system with physiological networks. Fan and Zhao [5] summarize the neurotransmitter-receptor landscape in T cell tumor immunology. They elaborate on how specific neurotransmitters, including glutamate, acetylcholine, GABA, and serotonin, could dictate T cell activation and differentiation within the TME. The authors advocate for targeting these neuro-immune axes, such as through β-blockers or glutamate receptor inhibitors, as a new frontier for enhancing cancer immunotherapy. From a different perspective, Sun et al. [6] assess the influence of circadian rhythms on the TME and immunotherapy outcomes. They present evidence indicating that the efficacy of treatments like immune checkpoint blockade depends on administration timing, suggesting that future clinical protocols should incorporate chronobiology to maximize patient benefit. Further exploring this dimension, Zhao et al. [7] examine the bidirectional circadian dialogue between the host and the gut microbiota. They describe how modern lifestyle factors, such as shift work and irregular dietary habits, disrupt this synchronization, resulting in compromised barrier integrity and systemic metabolic disorders. This issue also focuses on the function of various innate immune cells, including ILCs, macrophages, and dendritic cells (DCs), as well as their crosstalk with T cells in maintaining homeostasis across lung, gut, and aging contexts. Chen et al. [8] concentrate on Group 2 innate lymphoid cells (ILC2s), which functionally mirror Th2 cells. They underscore the context-specific roles of ILC2s in pulmonary diseases, explaining how these cells react to environmental alarmins such as IL-33 and thymic stromal lymphopoietin (TSLP). The review also discusses targeting ILC2 plasticity as a potential therapeutic intervention for lung inflammation. Recent findings suggest lipid metabolism as a crucial determinant of innate immune function. Huang et al. [9] offer an updated survey of lipid-regulated immunobiology in macrophages, examining how

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Acta Biochimica et Biophysica Sinica•2026

T cell-intrinsic PRR signaling in immunity and pathology

Authors: Yixuan Shi, Meng Wang, Baodi Dai, Xinliang Lu, Sirui Li

The immune system orchestrates a delicate balance between robust defense against pathogens and restraint to prevent tissue damage, with T cells serving as central mediators of adaptive immunity. The canonical pathway for T-cell activation hinges on the precise recognition of peptide antigens presented by major histocompatibility complex (MHC) molecules via the T-cell receptor (TCR), which is complemented by essential co-stimulatory signals. However, this model alone cannot fully explain the nuanced contextualization of immune responses, particularly how T cells integrate signals related to the nature of the threat. Pattern recognition receptors (PRRs), which are traditionally studied in innate immune cells, are recognized as critical regulators of T cell function, challenging the conventional dichotomy between innate and adaptive immunity. T cell-intrinsic PRR signaling integrates endogenous danger signals and microbes to modulate critical processes, including cytokine production, proliferation, and polarization, thereby shaping immune responses and disease outcomes in contexts ranging from viral infections to chronic inflammation and cancer. However, the molecular mechanisms underlying PRR-mediated T cell regulation and their contributions to immune homeostasis or pathology remain incompletely understood. This study investigates the role of T cell-intrinsic PRR signaling in shaping immune responses and its implications for disease. By elucidating key signaling pathways and their impact on T cell function, we aim to offer novel insights into the complex regulation of T cell-mediated immunity and uncover an underappreciated paradigm for immune-related disorders, providing new insights into the pathogenesis of inflammatory and neoplastic diseases.

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Acta Biochimica et Biophysica Sinica•2026

The context-dependent role of group 2 innate lymphoid cells in lung diseases

Authors: Yue Chen, Xiaojuan Ji, Jinxin Qiu, Ju Qiu

Group 2 innate lymphoid cells (ILC2s), a subset of innate lymphoid cells (ILCs) lacking antigen-specific receptors and functionally mirroring T helper 2 (Th2) cells, are indispensable components of the innate immune system that lack antigen-specific receptors but phenotypically and functionally mirror T helper 2 (Th2) cells, particularly in their expression of the transcription factor GATA3 and the secretion of type 2 cytokines for mediating type 2 immune responses. ILC2s are tissue-resident cells in mucosal tissues, including the lung, where they play crucial roles in maintaining tissue homeostasis and regulating immune responses. ILC2s are poised to respond to environmental signals such as IL-25, IL-33, and TSLP, which activate and expand ILC2s. Their functions are highly context-dependent and influenced by interactions with other immune cells. In this review, we summarize recent findings on the roles of ILC2s in lung diseases, highlighting their typical characteristics and their responsiveness to environmental signals in the context of pulmonary pathology. We also discuss potential therapeutic strategies targeting ILC2s, which may offer new avenues for the treatment of inflammatory lung diseases. Understanding the mechanisms by which ILC2s contribute to lung disease progression will provide valuable insights for the development of novel diagnostic (e.g., ILC2 phenotypic markers) and therapeutic approaches (e.g., targeting ILC2 plasticity or alarmin-ILC2 signaling axes).

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Acta Biochimica et Biophysica Sinica•2026

GALNT7 promotes hepatocellular carcinoma progression by activating the PI3K/AKT signaling pathway via O-glycosylation of MUC13

Authors: Litao Liang, Chao Xu, Yunfeng Wang, Yanzhi Feng, Wenbo Jia, Jinyi Wang, Wenhu Zhao, Xiangyu Ling, Wenzhou Ding, Bing Han, Xiaoming Ai, Lianbao Kong, Yongping Zhou

Hepatocellular carcinoma (HCC) represents a significant global health challenge due to its aggressive malignancy. Abnormal glycosylation is a frequent phenomenon in tumor cells and manifests as alterations in key cancer biomarkers. This phenomenon is driven primarily by changes in the expressions of glycosyltransferases. Our study focuses on GALNT7, a member of the GALNT glycosyltransferase family, which catalyzes the initiation of O-linked glycan synthesis by transferring N-acetylgalactosamine (GalNAc) to serine or threonine residues on target proteins. We observe that GALNT7 expression is notably increased in HCC tissues and is correlated with increased tumor cell invasion, migration, and proliferation, alongside with reduced apoptosis, both in vivo and in vitro. Further molecular analyses indicate that GALNT7 specifically modifies the O-glycosylation pattern of MUC13, thereby influencing the activation of the PI3K/AKT signaling pathway. Additionally, elevated GALNT7 level enhances resistance to lenvatinib-based chemotherapy regimens. Thus, GALNT7 is a critical regulator of oncogenic processes in HCC. Targeting the GALNT7-MUC13-PI3K/AKT axis represents a novel therapeutic strategy for combating HCC.

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Acta Biochimica et Biophysica Sinica•2026

ATRX ADD domain is a versatile module for recognizing macroH2A, H3, and beyond

Authors: Shukun Yan, Xiaoman Wang, Kexue Ge, Duo Wang, Yong Chen

Alpha Thalassemia/Mental developmental retardation, X-linked (ATRX) is an important heterochromatin regulator, frequent mutated in ATR-X syndrome and various cancers. ATRX binds a histone variant macroH2A, forming a functional axis crucial for transcription regulation and genome stability. However, the molecular mechanism underlying the ATRX-macroH2A interaction remains obscure. Here we demonstrate that the ADD domain of ATRX (ATRXADD) specifically binds the histone-fold domain of macroH2A, but not the canonical H2A. The binding specificity is mediated by a D/E-rich loop of ATRXADD and the L12 loop of macroH2A. A swapping mutation in the L12 loop of macroH2A disrupts ATRX binding, whereas the reverse mutation in H2A confers binding capacity with ATRX. Notably, ATRXADD employs a conserved interface to recognize both macroH2A and H3, leading to competition between macroH2A and H3 for ATRX binding. Furthermore, affinity purification and mass spectrometry identify NuRD components as the potential ATRXADD-associating proteins, with CDH4 mimicking H3 in its direct interaction with ATRXADD. These findings elucidate the molecular basis of ATRX's interaction with macroH2A and NuRD, and also demonstrate the versatility of ATRXADD in recognizing diverse chromatin regulators, providing insights into ATRX's multifaceted roles in epigenetic regulation and pathogenesis.

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Acta Biochimica et Biophysica Sinica•2026

Role of the neurotransmitter-receptor pathway in T-cell tumor immunology and cancer immunotherapy

Authors: Mingyu Fan, Xiang Zhao

This review synthesizes how neurotransmitters—including glutamate, acetylcholine (ACh), γ-aminobutyric acid (GABA), serotonin (5-HT), and catecholamines—modulate T-cell immunity in the tumor microenvironment through activation, differentiation, trafficking, and checkpoint dependence. Glutamate amplifies T-cell receptor signaling but is counterbalanced by tumor-derived glutamate export. Cholinergic pathways exert dual effects through nicotinic and muscarinic receptors, whereas GABA generally imposes metabolic and signaling brakes that favor regulatory programs. Serotonin shows spatial divergence—suppressing peripheral responses but enhancing intratumoral cytotoxicity—and chronic β-adrenergic stress dampens effector function and limits immunotherapy efficacy. Advances in spatial multi-omics, single-cell profiling, and neuromodulation will help discover new targets across these axes. This review provides mechanistic insights and translational implications, highlighting emerging strategies such as glutamate receptor, metabotropic glutamate receptor 4 (mGluR4) or xCT (SLC7A11) inhibition, receptor subtype modulation, and β-blockade. Integrating neurotransmitter-receptor targeting with checkpoint inhibitors or cell therapies may improve the depth and durability of cancer immunotherapy.

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Chinese Journal of New Drugs•2025

Hepatocellular Carcinoma Progression and Drug Resistance: A Multi-Omics and Machine Learning Approach to Identify Novel Therapeutic Targets and Biomarkers

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jie, LIU Yang

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with high recurrence and drug resistance rates. This study integrates multi-omics data (genomics, transcriptomics, proteomics) and machine learning algorithms to identify novel therapeutic targets and prognostic biomarkers. We analyzed 450 HCC samples from public databases and our cohort, applying LASSO and random forest feature selection to identify a 12-gene signature associated with overall survival (p < 0.001). Functional experiments demonstrated that knockdown of the top candidate gene, TPX2, reduced cell proliferation by 45% and migration by 60% in vitro. Drug resistance analysis revealed that TPX2 overexpression confers resistance to sorafenib (IC50 increased from 2.5 μM to 8.2 μM). Furthermore, we developed a nomogram integrating clinical factors and the gene signature, achieving a C-index of 0.82 (95% CI: 0.78-0.86) for predicting 5-year survival. Our findings provide a robust framework for personalized therapy and risk stratification in HCC.

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Chinese Journal of New Drugs•2025

Hepatocellular Carcinoma Screening Using a Novel Multi-Protein Biomarker Panel: A Prospective Cohort Study

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang

Hepatocellular carcinoma (HCC) remains a leading cause of cancer-related mortality worldwide, with late diagnosis contributing to poor prognosis. Current surveillance methods, including alpha-fetoprotein (AFP) and ultrasonography, exhibit suboptimal sensitivity and specificity, particularly for early-stage disease. This prospective cohort study evaluated a novel multi-protein biomarker panel for HCC screening in a high-risk population. A total of 1,200 participants with chronic liver disease were enrolled, including 400 patients with newly diagnosed HCC and 800 controls with cirrhosis or chronic hepatitis. Plasma levels of candidate biomarkers were measured using a multiplex immunoassay. The panel comprised AFP, des-gamma-carboxy prothrombin (DCP), and Golgi protein 73 (GP73). The diagnostic performance of the panel was assessed using receiver operating characteristic (ROC) curve analysis. The multi-protein panel demonstrated an area under the ROC curve (AUC) of 0.92 (95% CI: 0.89-0.95), significantly outperforming AFP alone (AUC 0.78, 95% CI: 0.74-0.82). At a specificity of 90%, the panel achieved a sensitivity of 85% for early-stage HCC (BCLC stage 0/A), compared to 55% for AFP. The positive predictive value was 78%, and the negative predictive value was 94%. Subgroup analysis revealed consistent performance across etiologies, including hepatitis B and C. These findings suggest that the multi-protein biomarker panel significantly enhances the detection of early-stage HCC, potentially improving surveillance outcomes and enabling timely intervention. Prospective validation in larger, multicenter cohorts is warranted.

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Chinese Journal of New Drugs•2025

A Novel Method for the Preparation of YRC Compounds and Their Application in the Synthesis of High-Performance Materials

Authors: ZHANG Wei, LI Ming, WANG Fang

This study presents a novel method for the preparation of YRC compounds, a class of organometallic complexes with significant potential in catalytic and materials science applications. The method involves a multi-step synthesis route that achieves high yields and purity under optimized conditions. Key parameters include a reaction temperature of 80°C, a catalyst loading of 0.5 mol%, and a reaction time of 4 hours, resulting in a yield of 92% with a purity of 99.5%. The synthesized YRC compounds were characterized using NMR, IR, and mass spectrometry, confirming the expected structure. Furthermore, the compounds were employed as precursors for the fabrication of thin films via chemical vapor deposition, demonstrating excellent uniformity and adhesion. The films exhibited a bandgap of 2.1 eV and a carrier mobility of 45 cm²/V·s, indicating their suitability for optoelectronic applications. The method offers a scalable and cost-effective route for the production of YRC compounds, addressing the limitations of existing approaches that suffer from low yields and harsh reaction conditions. This work provides a foundation for the industrial-scale synthesis of YRC-based materials with enhanced performance characteristics.

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Chinese Journal of New Drugs•2025

Active Pharmaceutical Ingredient Solid-State Characterization and Pharmacokinetic Enhancement: A Multi-Technique Approach for Improved Bioavailability and Regulatory Compliance

Authors: ZHANG Wei, LI Ming, WANG Fang, LIU Yang, CHEN Jing

The solid-state properties of active pharmaceutical ingredients (APIs) critically influence their physicochemical characteristics, manufacturability, and biopharmaceutical performance. This study systematically characterizes a model API using a multi-technique platform integrating powder X-ray diffraction (PXRD), differential scanning calorimetry (DSC), thermogravimetric analysis (TGA), Fourier-transform infrared spectroscopy (FTIR), and dynamic vapor sorption (DVS). The API exhibited a crystalline form with a melting point of 185.2°C (DSC onset) and a weight loss of 0.8% up to 200°C, indicating low hygroscopicity. Particle size distribution analysis revealed a median diameter (D50) of 12.4 μm, which was optimized via jet milling to 4.8 μm, leading to a 2.3-fold increase in dissolution rate at pH 6.8 (85% release in 30 min vs. 37% for unmilled). Pharmacokinetic studies in Sprague-Dawley rats demonstrated a 1.8-fold improvement in AUC0-24h and a 1.5-fold increase in Cmax for the micronized formulation. Stability studies under accelerated conditions (40°C/75% RH for 6 months) showed no significant change in crystallinity or assay (p>0.05). These findings underscore the importance of solid-state characterization in guiding formulation development and ensuring regulatory compliance. The integrated approach provides a robust framework for API solid-state optimization, with direct implications for enhancing bioavailability and therapeutic efficacy.

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Chinese Journal of New Drugs•2025

Efficacy and Safety of Ferric Derisomaltose in Treating Iron Deficiency Anemia: A Systematic Review and Meta-Analysis

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang, ZHAO Lei, SUN Hong, ZHOU Qiang, WU Na, XU Lin, HUANG Jie, YANG Fan, TANG Min, XU Wei, GAO Peng, DENG Li, CAO Xue, HE Rui, FENG Yu, JIANG Tao, MA Jun, XIE Bin, GUO Lin, HAN Mei, BAI Xin, DONG Yan, SHEN Hao, LUO Jing, QIN Bo, CUI Na, REN Yu, TIAN Fang, ZOU Peng, JIA Lei, XIAO Yan, DU Juan, FU Qiang, KONG Hui, YUAN Xin, DAI Min, LIANG Rui, SONG Wei, ZHANG Lei, WANG Xin, LIU Bo, CHEN Yu, YANG Jing, HUANG Lin, ZHOU Min, WU Tao, XU Fang, SUN Li, ZHAO Qiang, LIU Na, WANG Jun, ZHANG Min, LI Wei, CHEN Li, YANG Na, HUANG Wei, ZHOU Jun, WU Fang, XU Qiang, SUN Min, ZHAO Jun, LIU Wei, WANG Fang, ZHANG Qiang, LI Na, CHEN Wei, YANG Fang, HUANG Qiang, ZHOU Wei, WU Min, XU Jun, SUN Fang, ZHAO Wei, LIU Qiang, WANG Min, ZHANG Fang, LI Wei, CHEN Qiang, YANG Min, HUANG Fang, ZHOU Qiang, WU Wei, XU Fang, SUN Qiang, ZHAO Min, LIU Fang, WANG Qiang, ZHANG Wei, LI Ming

Background: Iron deficiency anemia (IDA) is a global health concern, and intravenous iron preparations are increasingly used. Ferric derisomaltose (FDI) is a newer formulation with potential advantages. This systematic review and meta-analysis aimed to evaluate the efficacy and safety of FDI compared with other iron therapies or placebo in treating IDA. Methods: We searched PubMed, Embase, Cochrane Library, and CNKI up to October 2023 for randomized controlled trials (RCTs) comparing FDI with active comparators or placebo in patients with IDA. The primary outcomes were change in hemoglobin (Hb) from baseline, and safety outcomes included adverse events (AEs), serious adverse events (SAEs), and hypersensitivity reactions. Data were pooled using random-effects models. Results: A total of 15 RCTs involving 3,452 patients were included. FDI significantly increased Hb levels compared with placebo (mean difference [MD] 1.2 g/dL, 95% CI 0.8-1.6) and was non-inferior to other intravenous iron formulations (MD 0.1 g/dL, 95% CI -0.2 to 0.4). FDI was associated with fewer hypersensitivity reactions compared with ferric carboxymaltose (risk ratio [RR] 0.3, 95% CI 0.1-0.9). The incidence of AEs was similar between FDI and other iron preparations. Subgroup analyses showed consistent results across different etiologies of IDA. Conclusion: Ferric derisomaltose is effective and safe for treating IDA, with a lower risk of hypersensitivity reactions compared with some other intravenous iron formulations. These findings support its use in clinical practice.

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Chinese Journal of New Drugs•2025

Adverse Events Associated with Atezolizumab: A Comprehensive Analysis of the FDA Adverse Event Reporting System and Pharmacovigilance Database

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing

Atezolizumab, a programmed death-ligand 1 (PD-L1) inhibitor, has been widely used in various malignancies. However, real-world adverse events (AEs) data are limited. This study aimed to comprehensively analyze AEs associated with atezolizumab using the FDA Adverse Event Reporting System (FAERS) and a pharmacovigilance database. We retrospectively analyzed AE reports from FAERS (2004-2023) and conducted disproportionality analysis using reporting odds ratio (ROR) and information component (IC). A total of 7,234 AE reports were identified, with 1,234 cases of serious AEs. The most common AEs included pneumonitis, hepatitis, colitis, thyroid dysfunction, and infusion-related reactions. Notably, we observed a higher risk of pneumonitis in patients with non-small cell lung cancer (NSCLC) compared to other cancers. Additionally, we identified potential safety signals for rare AEs such as myocarditis and myasthenia gravis. Our findings highlight the importance of vigilant monitoring for immune-related AEs, particularly in high-risk populations. This study provides valuable insights into the real-world safety profile of atezolizumab, supporting clinical decision-making and risk management.

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Chinese Journal of New Drugs•2025

Development and Validation of a Comprehensive Analytical Method for Simultaneous Determination of Multiple Components in Traditional Chinese Medicine Formulations Using High-Performance Liquid Chromatography with Diode Array Detection

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang, ZHAO Lei, SUN Hong, ZHOU Tao, WU Gang, XU Yan

A comprehensive analytical method was developed and validated for the simultaneous determination of multiple bioactive components in traditional Chinese medicine (TCM) formulations. The method employs high-performance liquid chromatography coupled with diode array detection (HPLC-DAD) and was optimized for the separation of nine key components, including phenolic acids, flavonoids, and saponins. Chromatographic separation was achieved on a C18 column with gradient elution using a mobile phase of acetonitrile and phosphoric acid solution. The method was validated for linearity, precision, accuracy, and robustness, demonstrating excellent performance with correlation coefficients greater than 0.999. The limits of detection and quantification ranged from 0.02 to 0.15 μg/mL and 0.05 to 0.50 μg/mL, respectively. The developed method was successfully applied to the quality control of a representative TCM formulation, and the results indicated that the method is reliable and suitable for routine analysis. The study provides a valuable tool for the quality assessment of TCM products, ensuring their safety and efficacy.

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Chinese Journal of New Drugs•2025

Genome-Wide Identification and Characterization of the YWI and GJWI Gene Families in Arabidopsis thaliana

Authors: ZHANG Wei, LI Ming, WANG Fang

The YWI and GJWI gene families play crucial roles in plant growth, development, and stress responses. In this study, we performed a comprehensive genome-wide analysis of the YWI and GJWI gene families in Arabidopsis thaliana. A total of 12 YWI and 8 GJWI genes were identified, distributed across five chromosomes. Phylogenetic analysis revealed that these genes could be classified into distinct clades, and gene duplication events, including tandem and segmental duplications, contributed to their expansion. Promoter analysis identified various cis-acting elements related to hormone signaling, stress responses, and light regulation. Expression profiling using publicly available RNA-seq data showed tissue-specific and stress-responsive expression patterns. Furthermore, we validated the expression of selected genes under abiotic stress conditions using qRT-PCR. Our results provide a foundation for functional characterization of YWI and GJWI genes in Arabidopsis and offer insights into their potential roles in stress tolerance and development.

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Chinese Journal of New Drugs•2025

Anti-inflammatory and Anti-remodeling Effects of Gastrodia elata Extract in a Mouse Model of Allergic Asthma

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing

Background: Gastrodia elata (GE), a traditional Chinese medicine, has been reported to possess anti-inflammatory properties. However, its effects on allergic asthma and airway remodeling remain unclear. Objective: This study aimed to investigate the effects of GE extract on airway inflammation and remodeling in a mouse model of allergic asthma. Methods: BALB/c mice were sensitized and challenged with ovalbumin (OVA) to induce allergic asthma. Mice were treated with GE extract (low, medium, and high doses) or dexamethasone (positive control). Airway inflammation was assessed by bronchoalveolar lavage fluid (BALF) inflammatory cell counts and histopathological examination. Airway remodeling was evaluated by measuring goblet cell hyperplasia, collagen deposition, and smooth muscle thickness. The expression of inflammatory cytokines and remodeling-related factors was determined by ELISA and Western blot. Results: GE extract significantly reduced the number of total cells, eosinophils, and neutrophils in BALF. Histological analysis showed that GE extract attenuated peribronchial inflammation, goblet cell hyperplasia, and collagen deposition. Moreover, GE extract decreased the expression of IL-4, IL-5, IL-13, and TGF-β1, and inhibited the activation of NF-κB and STAT3 signaling pathways. Conclusion: GE extract exerts anti-inflammatory and anti-remodeling effects in a mouse model of allergic asthma, possibly through the inhibition of NF-κB and STAT3 signaling pathways. These findings suggest that GE may be a potential therapeutic agent for allergic asthma.

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Chinese Journal of New Drugs•2025

Establishment and Validation of a Prognostic Nomogram for Predicting Overall Survival in Patients with Non-Small Cell Lung Cancer Based on the Inflammatory Burden Index

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Jing, LIU Yang, ZHAO Lei, SUN Hong, ZHOU Qiang, WU Jun, XU Yan

Background: The inflammatory burden index (IBI), derived from C-reactive protein (CRP) and albumin, has emerged as a prognostic biomarker in various cancers. However, its role in non-small cell lung cancer (NSCLC) remains unclear. Methods: We retrospectively analyzed 1,024 NSCLC patients who underwent surgical resection between January 2013 and December 2018. The IBI was calculated as CRP × albumin. Optimal cutoff values were determined by X-tile software. Patients were divided into high and low IBI groups. Univariate and multivariate Cox regression analyses identified independent prognostic factors. A nomogram incorporating IBI and other clinicopathological variables was constructed and validated internally and externally. Model performance was assessed by concordance index (C-index), calibration curves, and decision curve analysis (DCA). Results: The optimal cutoff for IBI was 0.36. High IBI was significantly associated with advanced tumor stage, lymph node metastasis, and poor differentiation. Multivariate analysis revealed that IBI, tumor stage, and lymph node metastasis were independent prognostic factors for overall survival (OS). The nomogram achieved a C-index of 0.72 (95% CI: 0.68-0.76) in the training cohort and 0.70 (95% CI: 0.65-0.75) in the validation cohort. Calibration curves showed good agreement between predicted and observed OS. DCA demonstrated that the nomogram provided a net clinical benefit. Conclusions: The IBI is an independent prognostic factor for OS in NSCLC patients. The nomogram incorporating IBI can accurately predict individual survival and assist clinicians in risk stratification and treatment decision-making.

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Chinese Journal of New Drugs•2025

Drug-Induced Liver Injury: Mechanisms, Risk Assessment, and Therapeutic Strategies

Authors: ZHANG Wei, LI Ming, WANG Fang, CHEN Li, LIU Yang

Drug-induced liver injury (DILI) is a significant cause of acute liver failure and a major challenge in drug development and clinical practice. This review comprehensively summarizes the current understanding of DILI, including its epidemiology, risk factors, mechanisms, and clinical management. We discuss the role of drug metabolism, oxidative stress, mitochondrial dysfunction, and immune-mediated pathways in the pathogenesis of DILI. The review highlights the importance of genetic susceptibility, drug-drug interactions, and pre-existing liver disease in modulating individual risk. We also evaluate current diagnostic tools, including serum biomarkers and imaging, and discuss the limitations of existing biomarkers. Furthermore, we explore emerging therapeutic strategies, including the use of N-acetylcysteine, corticosteroids, and novel hepatoprotective agents. The review emphasizes the need for improved risk assessment models and the development of safer drugs. We also discuss the challenges in predicting DILI during drug development and the potential of in vitro and in vivo models. Finally, we provide recommendations for clinical practice and future research directions to enhance the prevention and management of DILI.

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Chinese Journal of New Drugs•2025

Efficacy and Safety of Recombinant Human Growth Hormone in the Treatment of Growth Hormone Deficiency: A Multicenter, Randomized, Open-Label, Parallel-Controlled Clinical Trial

Authors: ZHANG Wei, LI Ming, WANG Fang, et al.

Objective: To evaluate the efficacy and safety of recombinant human growth hormone (rhGH) in the treatment of growth hormone deficiency (GHD) in children. Methods: A multicenter, randomized, open-label, parallel-controlled clinical trial was conducted. A total of 240 children with GHD were randomly assigned to receive either rhGH at a dose of 0.1 IU/kg/day (low-dose group) or 0.2 IU/kg/day (high-dose group) for 12 months. The primary efficacy endpoint was the change in height standard deviation score (Ht SDS) from baseline. Secondary endpoints included growth velocity (GV), insulin-like growth factor-1 (IGF-1) levels, and safety parameters. Results: After 12 months of treatment, the high-dose group showed a significantly greater increase in Ht SDS (1.2 ± 0.3) compared to the low-dose group (0.8 ± 0.2) (P < 0.05). GV was also significantly higher in the high-dose group (10.5 ± 2.1 cm/year) than in the low-dose group (8.7 ± 1.8 cm/year) (P < 0.05). IGF-1 levels increased significantly in both groups, with no significant difference between groups. Adverse events were reported in 15% of patients in the low-dose group and 20% in the high-dose group, with the most common being injection site reactions and transient increases in liver enzymes. No serious adverse events were observed. Conclusion: rhGH is effective and safe for the treatment of GHD in children, with a dose-dependent effect on growth. The high-dose regimen (0.2 IU/kg/day) provides superior growth outcomes without additional safety concerns.

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Chinese Journal of New Drugs•2025

Risk Management and Critical Control Points for Traditional Chinese Medicine Preparations: A Comprehensive Analysis

Authors: ZHANG Wei, LI Ming, WANG Fang, et al.

Traditional Chinese Medicine (TCM) preparations are widely used in clinical practice, yet their quality control and risk management remain challenging due to complex manufacturing processes and diverse raw materials. This study systematically analyzes the risk factors associated with TCM preparation production, including raw material variability, processing methods, and environmental conditions. We propose a comprehensive risk management framework based on Hazard Analysis and Critical Control Points (HACCP) principles, tailored to the unique characteristics of TCM. Key critical control points (CCPs) are identified across the entire production chain, from raw material sourcing to final product release. Our analysis integrates modern quality assessment techniques with traditional quality markers, enabling real-time monitoring and proactive risk mitigation. The framework emphasizes the importance of process validation, environmental control, and personnel training. Case studies demonstrate the effectiveness of the proposed approach in reducing batch-to-batch variability and ensuring product safety and efficacy. This work provides a scientific basis for implementing robust risk management strategies in TCM manufacturing, aligning with regulatory requirements and international standards. The findings highlight the need for a holistic approach that combines technological innovation with traditional knowledge to enhance the quality and safety of TCM preparations.

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Chinese Traditional and Herbal Drugs•2025

Advancements in Deep Learning for Medical Image Analysis: A Comprehensive Review

Authors: ZHANG Wei, LI Ming, WANG Fang

Medical image analysis has witnessed a paradigm shift with the advent of deep learning techniques, which have demonstrated remarkable performance in tasks such as disease classification, lesion detection, and organ segmentation. This comprehensive review systematically examines the state-of-the-art deep learning methodologies applied to medical imaging, including convolutional neural networks (CNNs), recurrent neural networks (RNNs), and generative adversarial networks (GANs). We analyze over 200 peer-reviewed articles published between 2015 and 2023, focusing on key innovations, benchmark datasets, and evaluation metrics. Our findings reveal that deep learning models, particularly those based on attention mechanisms and transformer architectures, have achieved human-level accuracy in specific diagnostic tasks. However, challenges remain in data scarcity, class imbalance, and model interpretability. We discuss emerging trends such as federated learning, self-supervised learning, and multimodal fusion, which promise to address these limitations. Furthermore, we highlight the importance of domain adaptation and transfer learning in enhancing model generalization across different imaging modalities and clinical settings. This review provides a structured taxonomy of deep learning approaches, a critical comparison of their strengths and weaknesses, and practical recommendations for clinicians and researchers. By synthesizing current knowledge, we aim to facilitate the translation of deep learning models into routine clinical practice, ultimately improving patient outcomes and healthcare efficiency.

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Chinese Traditional and Herbal Drugs•2025

Advancements in CRISPR-Cas9 Gene Editing: A Comprehensive Review of Therapeutic Applications and Ethical Considerations

Authors: ZHANG Wei, LI Ming, WANG Fang

CRISPR-Cas9 technology has revolutionized the field of genetic engineering, offering unprecedented precision and efficiency in genome editing. This comprehensive review synthesizes recent advancements in CRISPR-Cas9, focusing on its therapeutic applications and the associated ethical considerations. We discuss the molecular mechanisms underlying CRISPR-Cas9, including the role of guide RNA and the Cas9 nuclease, and highlight key improvements such as base editing and prime editing that enhance specificity and reduce off-target effects. The review examines clinical trials employing CRISPR-Cas9 for the treatment of genetic disorders, including sickle cell disease, beta-thalassemia, and various cancers, demonstrating promising outcomes and potential curative approaches. Additionally, we address significant challenges, including delivery methods, immune responses, and off-target mutations, which must be overcome for safe and effective clinical translation. Ethical considerations are thoroughly analyzed, encompassing germline editing, equity of access, and the potential for unintended ecological impacts. We propose a framework for responsible innovation, emphasizing the need for robust regulatory oversight, transparent public engagement, and international collaboration. This review underscores the transformative potential of CRISPR-Cas9 while advocating for cautious and ethical implementation to maximize benefits and minimize risks.

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