Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04921-w
Background Lung ischemia–reperfusion injury (IRI) is a major contributor to primary graft dysfunction (PGD) after lung transplantation. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have emerged as promising therapeutic agents in inflammatory diseases by ameliorating tissue damage and promoting repair. However, the anti-inflammatory efficacy of these approaches and the underlying mechanisms in lung ischemia–reperfusion injury remain incompletely understood. Methods The protective effects of mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) against lung ischemia–reperfusion injury were evaluated using two delivery approaches, inhalation and intravenous injection. Both in vivo and in vitro models were employed to assess the biological activity of MSC-EVs and to elucidate the underlying molecular mechanisms. In addition, a rat orthotopic lung transplantation (OLT) model was established to further examine the translational relevance of MSC-EVs. Results MSC–EVs treatment significantly ameliorated lung IRI, with inhalation showing superior efficacy over intravenous delivery. Mechanistically, miR-22-3p within MSC-EVs targeted macrophage NLRP3, suppressing activation of the NLRP3/Caspase-1/IL-1β pathway and promoting M2 polarization. The protective efficacy was confirmed in a clinically relevant rat OLT model, underscoring their translational potential
Stem Cell Research & Therapy•2024•DOI: 10.1186/s13287-024-03949-0
Background The selection of suitable culture medium is critical for achieving good clinical outcomes in cell therapy. To support the commercial application of stem cell therapy, customized culture media not only need to promote stem cell proliferation, but also need to save costs and meet industrial requirements for inter-batch consistency, efficacy, and biosafety. In this study, we developed a series of serum-free media (SFM) and elucidated the effects between different SFM, as well as between SFM and serum-containing meida (SCM), on human umbilical cord mesenchymal stem cells (hUC-MSCs) phenotype and function. We analyze and emphasize from the perspectives of clinical and commercial application why research on customized culture media is critical for the success of enterprises developing novel cellular therapeutics. Methods We cultured hUC-MSCs with identical cell seeding densities in different formulations of SFM and SCM until passage 10 and examined the changes in cell phenotype and function. We analyzed the results with the commercial application requirments of the cellular therapy industry to assess the potential impact of customized culture media on inter-batch consistency, efficacy, stability, biosafety, and cost-effectiveness of industrial-scale cell production. Results hUC-MSCs cultured in SCM and SFM exhibit consistent cell morphology and surface molecule expression, but hUC-MSCs cultured in SFM demonstrate higher activity, superior proliferative capacity, and greater stability. Furthermore, hUC-MSCs cultured in different SFM exhibit differences in cell activity, proliferative capacity, senescent rate, and S/M ratio of cell cycle, while maintaining a normal karyotype after long-term in vitro cultivation. Moreover, [abstract truncated]
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024215
A better understanding of how sympathetic nerves impact pancreatic function is helpful for understanding diabetes. However, there is still uncertainty and controversy surrounding the roles of sympathetic nerves within the pancreas. To address this, we utilize high-resolution imaging and advanced three-dimensional (3D) reconstruction techniques to study the patterns of sympathetic innervation and morphology in the islets of adult wild-type (WT) and diabetic mice. Our data show that more than ~30% of α/β-cells are innervated by sympathetic nerves in both WT and diabetic mice. Additionally, sympathetic innervated α/β-cells are reduced in diet-induced obese (DIO) mice, whereas sympathetic innervated β-cells are increased in db/db mice. In addition, in situ chemical pancreatic sympathetic denervation (cPSD) improves glucose tolerance in WT and db/db mice but decreases glucose tolerance in DIO mice. In situ cPSD also enhances insulin sensitivity in diabetic mice without affecting WT mice. Overall, our findings advance our understanding of diabetes by highlighting the distinctive impact of pancreatic sympathetic innervation on glucose regulation.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025048
As a classic tumor suppressor gene, p53 has been extensively studied since its discovery in the mid-1980s. Research findings have revealed that p53 protein expression is suppressed in various cancers [1]. For example, in cervical cancer, p53 predominantly exists in a wild-type form to maintain its biological function [2]. Nevertheless, its tumor-suppressive activity is significantly impaired because of rapid protein degradation, short half-life, and low levels. Post-translational modifications (PTMs) of p53, such as ubiquitination, acetylation, phosphorylation and methylation, are critical regulators of its stability, activity, conformation, localization, and interactions with cofactors [3]. Among these, ubiquitination and acetylation play central roles in controlling p53 protein stability and activity [4]. Therefore, targeting p53 PTMs to modulate its ubiquitination and acetylation levels represents an effective strategy to increase its stability and tumor-suppressive function, offering a promising avenue for cervical cancer drug development. In 99% of cervical cancers (high-risk human papillomavirus-positive), E3 ubiquitin ligase E6-associated protein (E6AP) mediates the ubiquitination degradation of p53 [5], whereas histone deacetylase 6 (HDAC6) deacetylates p53. In this study, we explored the possibility of combining the natural product withferin A (WA) with the HDAC6 inhibitor ricolinostat (RIC) to treat cervical cancer cells, with a focus on the ubiquitination and acetylation of p53 and the consequences for its stability. These results suggested that the combination of WA and RIC is more effective than either treatment alone in inhibiting the degradation and increasing the stability of p53, thereby synergistically slowing the onset and progression of cervical cancer.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025094
Kainate receptors (KARs) are one of the ionotropic glutamate receptor (iGluR) families, and their antagonists are being investigated for the treatment of several neurological disorders, including Alzheimer’s disease, a neurodegenerative condition, etc. As early as 1990, Bettler et al. [1] first cloned the GRIK1 subunit of KARs, marking a pivotal advancement in understanding these receptors. Members of the iGluR family have been identified in other jawed vertebrates and exhibit conserved structural features. However, research into iGluRs in jawless vertebrates has been limited. Owing to the unique evolutionary position of lampreys, their iGluRs might also present functions distinct from those of jawed vertebrates; therefore, it is particularly important to study iGluRs in lampreys. In this study, we identified four homologous subunits of iGluRs in lampreys, including Lr-GRIA2, Lr-GRIA4, Lr-GRIK1 and Lr-GRIN2B. Lampreys occupy a unique evolutionary position, making phylogenetic analysis of iGluR subunits between lampreys and other species essential for understanding iGluR evolution. Given the distinctive functional characteristics of iGluR family members, particularly KAR subtypes, we focused on the functional validation of Lr-GRIK1. First, we confirmed the expression of Lr-GRIK1 in lampreys and examined its expression profiles across various tissues via qPCR and western blotting. To elucidate the functional role of Lr-GRIK1 in lampreys, we used an siRNA to silence Lr-GRIK1. We subsequently conducted transcriptome sequencing of both the silenced and control groups to construct and analyze their expression profiles. Our analysis revealed differential expression of genes enriched in pathways related to signal transduction and the immune system, highlighting potential roles of Lr-GRIK1 beyond traditional neurotransmission functions. Unlike in jawed vertebrates, transcriptome enrichment provides a new direction for understanding the function of Lr-GRIK1. Therefore, we monitored the changes in Lr-GRIK1 expression in the kidney tissue of lampreys after stimulation. In addition, we confirmed that Lr-GRIK1 affects the expression levels of immune-related molecules during the immune response process. These findings provide insights into the broader functional significance of Lr-GRIK1 in the biology of lampreys.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026081
Multiple myeloma (MM) patients frequently experience relapse, disease progression, and drug resistance, necessitating novel therapeutic strategies. This study investigates the role of peptidylprolyl isomerase A (PPIA) in mediating dihydroartemisinin (DHA)-induced ferroptosis in MM. Building on our previous work establishing the prognostic relevance of ferroptosis in MM, we elucidate the mechanism by which DHA triggers this form of cell death through the disruption of iron metabolism and redox homeostasis. DHA significantly reduces the viability of MM cell lines and primary CD138+ cells derived from patient bone marrow samples and attenuates tumor burden in orthotopic MM models. Mechanistically, DHA upregulates the iron-regulatory genes transferrin receptor 1 (TFRC) and heme oxygenase-1 (HMOX1), thereby perturbing iron homeostasis and promoting ferroptosis. Crucially, DHA targets the oxidized form of PPIA, a redox-sensitive chaperone, binding to it and preventing its reduction, which elevates intracellular reactive oxygen species (ROS). Combined treatment with DHA and erastin, which concurrently disrupt iron and amino acid metabolism, exerts synergistic cytotoxicity and enhances MM inhibition. Furthermore, in a syngeneic mouse model, DHA promotes T-cell activation and augments tumor suppression. Collectively, these findings underscore PPIA’s pivotal role in a novel ferroptotic cell death pathway and reveal new therapeutic opportunities for MM.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026027
Phosphorylated CTD Interacting Factor 1 (PCIF1) is the exclusive methyltransferase responsible for the N6,2-O-dimethyladenosine (m6Am) modification in mammalian mRNA. Our previous research identified PCIF1 as a potent tumor suppressor in glioma, demonstrating its ability to impair cell proliferation, induce G2/M phase arrest, and promote apoptosis. However, its role in glioma cell migration and invasion remains unclear. In this study, we investigate how PCIF1 regulates glioma cell migration and invasion. Overexpression of PCIF1 inhibits migration and invasion, whereas PCIF1 knockdown enhances these behaviors. Corresponding changes are observed in mesenchymal markers (Vimentin, β-catenin, Snail, Slug) and the epithelial marker T-cadherin, indicating that PCIF1 suppresses epithelial-to-mesenchymal transition (EMT)-mediated glioma invasion. Mechanistically, PCIF1 modulates the AKT pathway by promoting proteasomal degradation of AKT while increasing phosphorylated AKT (p-AKT) levels, revealing a complex regulatory mechanism. PCIF1 knockdown upregulates INPP5B, a lipid phosphatase, causing accumulation of PI(3,4)P2 and enhanced AKT activation. Conversely, PCIF1 overexpression increases PI(3,4,5)P3 production, elevating p-AKT levels. This bidirectional regulation suggests that PCIF1 influences phosphoinositide signaling and AKT activation. Our findings highlight PCIF1 as a key modulator of glioblastoma cell migration and invasion through phosphoinositide signaling, positioning it as a potential biomarker and therapeutic target in glioma.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2024213
Approximately one-tenth of the global population is affected by diabetes mellitus, and its incidence continues to rise each year. In China, 1.4 million patients die of diabetes-related complications every year. Additionally, approximately 26% of patients with diabetes develop diabetic cardiomyopathy, with heart failure being one of the main causes of death in these patients. However, early detection of diabetic cardiomyopathy has proven to be difficult in a clinical setting; furthermore, there are limited guidelines and targeted means of prevention and treatment for this disease. In recent years, several studies have provided evidence for the occurrence of various forms of regulated cell death in diabetic myocardial cells, including apoptosis, necroptosis, ferroptosis, and cuproptosis, which are closely linked to the pathological progression of diabetic cardiomyopathy. Although most research on diabetic cardiomyopathy is currently in the animal trial phase, the inhibition of these regulatory cell death processes can limit or slow down the progression of diabetic cardiomyopathy. Therefore, this review discusses the appropriate animal experimental models currently available for diabetic cardiomyopathy and evaluates the roles of apoptosis, necroptosis, ferroptosis, and cuproptosis in diabetic cardiomyopathy. We hope to provide new methods and ideas for future research in diabetic cardiomyopathy.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2025139
Sepsis-associated acute liver injury (SALI) is a frequent and clinically severe complication of sepsis, in which inflammatory responses and oxidative stress are involved. Angelicin (ANG), one of the main active components in the traditional Chinese medicine Psoralea corylifolia Linn., has anti-inflammatory and antioxidant bioactivities. In this study, the protective effect of ANG on SALI and its specific mechanism are investigated by establishing a mouse model of caecal ligation and puncture (CLP)-induced SALI and an in vitro sepsis model in LPS-stimulated AML12 cells. These results show that ANG can alleviate liver injury and improve liver function in SALI mice. ANG decreases the mRNA expression levels of the pro-inflammatory factors Il-1β, Il-6, and Tnf-α and increases the mRNA expression level of the anti-inflammatory factor Il-10, which suggests its anti-inflammatory effects. The results of the biochemical kit assay and DHE staining show that ANG can decrease the levels of MDA and ROS and increase the level of GSH and the activities of CAT and SOD, which suggests that ANG has antioxidant effects. Mechanistically, ANG exerts anti-inflammatory effects by inhibiting the NF-κB and p38 MAPK pathways and exerting antioxidant effects by activating the Nrf2/Keap1 pathway. Additionally, cell transfection experiments indicate that activation of the Nrf2/Keap1 pathway by ANG may depend on the inhibition of the NF-κB pathway. In conclusion, ANG attenuates SALI by inhibiting the NF-κB and p38 MAPK pathways, thereby activating the Nrf2/Keap1 pathway and making it a promising therapeutic intervention for SALI.
Acta Biochimica et Biophysica Sinica•2024•DOI: 10.3724/abbs.2024121
Gene regulation refers to the precise regulation of gene expression in an organism, and transcription factors are proteins that bind to DNA and regulate gene expression by promoting or inhibiting the expressions of target genes. Since the late 1980s [1], scientists have studied special genes called Pax genes that control how genes function in organisms as they grow. There are nine Pax genes found in animals such as mice, zebrafish, and humans [2]. Based on the composition domain and homology of the sequence, the Pax family is divided into four subfamilies: Pax1/9, Pax2/5/8, Pax4/6, and Pax3/7 [3]. Pax7 plays a pivotal role in the implementation, protection, and repair of skeletal muscle. Pax7 helps to control the balance between self-renewal and differentiation of satellite cells, ensuring that they can proliferate when needed to generate new muscle cells and differentiate into mature muscle fibers when necessary for muscle development and repair. The expression of the Pax7 gene in nerve cells is critical for dorsal root and sensory ganglia development. The Pax7 gene serves as a primary controlling factor for skeletal muscle development while influencing different biological processes; however, its exact role in jawless vertebrates such as lamprey remains unclear, and extensive research is needed to elucidate the intricate underlying mechanisms involved. Given the unique status of lamprey as an ancient jawless fish, possessing an ancient lineage and distinctive biological features, it is rare to explore gene function across hundreds of millions of years of vertebrate evolution. The use of lamprey as a model system for gene function research represents an innovative approach in the fields of evolutionary and comparative genomics. In this study, we investigated the regulatory mechanism of Pax7 in lamprey via gene cloning, gene expression analysis, gene silencing and transcriptome data analysis. We also explored the interactions between genes with significant differences. Identification of Lr.Pax7 in lamprey tissues began with the retrieval of protein sequences that are similar to those of human Pax family members in sea lamprey (Petromyzon marinus) or zebrafish (Danio rerio) from the NCBI protein database (Supplementary Table S1) and the use of BLAST to identify corresponding homologs (Supplementary Table S2). Subsequently, we extracted the Pax sequences from our library. Lethenteron reissneri specimens were dissected to isolate various tissues. Primers targeting the pax domains were designed based on the Pax7 nucleotide sequence in the Lampreys cDNA library, and the aim was to verify the effectiveness of the Lampreys cDNA as a template for validation (Supplementary Table S3). Lr.Pax7 was successfully amplified via PCR in muscle tissue. Here, a variety of methods were used for bioinformatics analysis. The results showed that the amino acid sequence of Pax7 is highly similar among animals (Figure 1A), with a decreasing trend from higher to lower organisms, as revealed by sequence alignment. It can be observed from the evolutionary tree (Figure 1B) that Pax genes for each subfamily are present in ancestral chordate and that Pax genes are present in amphioxus. Petromyzon marinus, Lethenteron camtschaticum, and Lethenteron reissneri constitute a sister group and have become good models for the study of jawless vertebrates. Pax9, Pax2, Pax6, and Pax7 show high similarity to those of other higher vertebrates. Therefore, these genes were named Lr.Pax9, Lr.Pax2, Lr.Pax7, and Lr.Pax6. The results indicate that the Pax7 gene is significantly preserved across various species, from higher to lower. This suggests that the DNA sequence of the gene is remarkably similar among different species. Lr.Pax7 is positioned between vertebrates and invertebrates and is most closely related to P. marinus Pax7. This finding provides more insight into the original evolutionary position of the lamprey. Crystal structure prediction analysis revealed that Lr.Paxs and Hm.Paxs have highly homologous structures (Figure 1C). The Pax gene has a similar structure (Figure 1D), including a conserved DNA-binding structure called the pair-box domain. This structure contains approximately 128 amino acids and is responsible for binding with specific DNA sequences, regulating gene expression, and interacting with other proteins. To further investigate the evolutionary history of Pax7 in vertebrates, we compared the genetic environment of Pax7 with that of other vertebrates (Figure 1E). In addition, many Pax gene members also contain DNA-binding structures called homeodomains, which play important roles in development.
Stem Cell Research & Therapy•2026•DOI: 10.1186/s13287-026-04921-w
Lung ischemia-reperfusion injury (IRI) remains the principal driver of primary graft dysfunction (PGD) following transplantation, with no approved pharmacological prophylaxis. This study evaluated mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) delivered by inhalation versus intravenous injection in murine hilar clamp and rat orthotopic lung transplantation (OLT) models. Inhalation achieved superior attenuation of pulmonary injury relative to systemic administration. Mechanistically, MSC-EV-encapsulated miR-22-3p was delivered to alveolar macrophages, where it targeted NLRP3 and suppressed the ASC/Caspase-1/IL-1β axis, reducing pyroptosis and promoting M2 polarization. These effects lowered cytokine-driven damage and enhanced tissue repair. Efficacy was confirmed in a clinically relevant rat OLT model, supporting translational potential for PGD prevention. The findings establish a pathway-specific, cell-free therapeutic strategy with a favorable route-dependent efficacy profile.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026081
Multiple myeloma (MM) patients frequently experience relapse, disease progression, and drug resistance, necessitating novel therapeutic strategies. This study investigates the role of peptidylprolyl isomerase A (PPIA) in mediating dihydroartemisinin (DHA)-induced ferroptosis in MM. Building on our previous work establishing the prognostic relevance of ferroptosis in MM, we elucidate the mechanism by which DHA triggers this form of cell death through the disruption of iron metabolism and redox homeostasis. DHA significantly reduces the viability of MM cell lines and primary CD138+ cells derived from patient bone marrow samples and attenuates tumor burden in orthotopic MM models. Mechanistically, DHA upregulates the iron-regulatory genes transferrin receptor 1 (TFRC) and heme oxygenase-1 (HMOX1), thereby perturbing iron homeostasis and promoting ferroptosis. Crucially, DHA targets the oxidized form of PPIA, a redox-sensitive chaperone, binding to it and preventing its reduction, which elevates intracellular reactive oxygen species (ROS). Combined treatment with DHA and erastin, which concurrently disrupt iron and amino acid metabolism, exerts synergistic cytotoxicity and enhances MM inhibition. Furthermore, in a syngeneic mouse model, DHA promotes T-cell activation and augments tumor suppression. Collectively, these findings underscore PPIA's pivotal role in a novel ferroptotic cell death pathway and reveal new therapeutic opportunities for MM.
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026027
Phosphorylated CTD Interacting Factor 1 (PCIF1) is the exclusive methyltransferase responsible for the N6,2-O-dimethyladenosine (m6Am) modification in mammalian mRNA. Our previous research identified PCIF1 as a potent tumor suppressor in glioma, demonstrating its ability to impair cell proliferation, induce G2/M phase arrest, and promote apoptosis. However, its role in glioma cell migration and invasion remains unclear. In this study, we investigate how PCIF1 regulates glioma cell migration and invasion. Overexpression of PCIF1 inhibits migration and invasion, whereas PCIF1 knockdown enhances these behaviors. Corresponding changes are observed in mesenchymal markers (Vimentin, β-catenin, Snail, Slug) and the epithelial marker T-cadherin, indicating that PCIF1 suppresses epithelial-to-mesenchymal transition (EMT)-mediated glioma invasion. Mechanistically, PCIF1 modulates the AKT pathway by promoting proteasomal degradation of AKT while increasing phosphorylated AKT (p-AKT) levels, revealing a complex regulatory mechanism. PCIF1 knockdown upregulates INPP5B, a lipid phosphatase, causing accumulation of PI(3,4)P2 and enhanced AKT activation. Conversely, PCIF1 overexpression increases PI(3,4,5)P3 production, elevating p-AKT levels. This bidirectional regulation suggests that PCIF1 influences phosphoinositide signaling and AKT activation. Our findings highlight PCIF1 as a key modulator of glioblastoma cell migration and invasion through phosphoinositide signaling, positioning it as a potential biomarker and therapeutic target in glioma.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21252
BACKGROUND: The occurrence of major depressive disorder is typically associated with genetic and environmental factors. Currently, the diagnosis of major depressive disorder mainly relies on clinical interviews and symptom assessments, lacking clear and reproducible biological markers. This can lead to misdiagnosis and missed diagnoses, delaying the timing of treatment. OBJECTIVE: To identify druggable genes that may act as potential therapeutic targets for major depressive disorder by conducting comprehensive genome-wide Mendelian randomization analysis. METHODS: By integrating expression quantitative trait locus (eQTL) data and protein quantitative trait locus (pQTL) data from pharmacologically actionable genes with genome-wide association study (GWAS) data on major depressive disorder (including 177 377 cases and 445 321 controls), Mendelian randomization analysis was conducted to identify druggable genes that have a causal relationship with major depressive disorder. Additionally, enrichment analysis, protein-protein interaction network construction, drug target identification, and molecular docking simulations were performed to further explore potential therapeutic strategies. RESULTS AND CONCLUSION: A total of 4 394 druggable genes were analyzed, and 21 druggable genes considerably associated with major depressive disorder were identified. Bayesian colocalization analysis indicated that BTN3A3, CISD1, and PSMB4 had posterior probabilities of hypothesis 4 (H4.abf) > 0.5, supporting the possibility of shared causal variants. GO enrichment analysis mainly involved 'antigen processing and presentation', 'protein degradation and processing', 'mitochondrial outer membrane', and 'immune receptor activity' pathways related to major depression. Protein-protein interaction network analysis showed moderate connectivity among the identified genes (21 nodes, 14 edges). Drug target identification determined gemcitabine (CID 60750), fucose (CID 17106), and isococculidine (CID 2826) as main candidate compounds, which had strong associations with several key genes. Molecular docking analysis revealed stable drug-protein interactions, with isococculidine showing the most stable binding energy (-52.74 kJ/mol) with BTN3A3. In conclusion, Mendelian randomization combined with genomics and structural biology analysis provides valuable decision-making basis for target prioritization and drug repurposing, offering new ideas and directions for efficient utilization of basic research resources and drug development for major depressive disorder.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21287
BACKGROUND: The onset of cervical instability in middle-aged and young adults often begins with neck muscle injuries. A deeper understanding of changes in neck muscles during cervical instability and their correlation can provide valuable data to support the prevention and treatment of cervical instability in this population. OBJECTIVE: To explore the correlation between cervical instability and neck muscle changes in middle-aged and young adults. METHODS: A total of 98 patients with cervical C4/5 instability and 88 healthy subjects, aged 18-45 years, were enrolled through recruitment advertisements and the Department of Spine, Wangjing Hospital, China Academy of Traditional Chinese Medicine. Cervical X-rays were collected to measure cervical curvature and C4/5 vertebral angular displacement. Cervical magnetic resonance imaging was taken to obtain data on C4/5 intervertebral disc signal intensity, as well as the relative cross-sectional area and fat ratio of neck muscles, including prevertebral muscles, deep posterior cervical muscles, and superficial muscles. A univariate intergroup comparison of X-ray and magnetic resonance imaging data was conducted between cervical instability subjects and healthy controls, along with Spearman correlation analysis between C4/5 angular displacement and disc signal intensity, relative cross-sectional area of neck muscles and fat percentage at the C4/5 level in cervical instability patients. RESULTS AND CONCLUSION: The cervical instability group had significantly greater age, C4/5 horizontal displacement, C4/5 angular displacement, and fat ratio of deep posterior cervical muscles than the healthy group (P < 0.05), while cervical curvature and relative cross-sectional area of deep posterior cervical muscles were significantly smaller (P < 0.05). Spearman correlation analysis showed a negative correlation between C4/5 angular displacement and relative cross-sectional area of deep posterior cervical muscles (P < 0.05). These findings suggest that changes in deep posterior cervical muscles may be closely related to the occurrence of cervical instability in middle-aged and young adults.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21382
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.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21486
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.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21527
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.
Chinese Journal of Tissue Engineering Research•2026•DOI: 10.12307/2026.21605
OBJECTIVE: To systematically evaluate the effects of motor imagery-based brain-computer training on upper limb motor function in patients with stroke, thereby providing evidence-based guidance for clinical practice. METHODS: The randomized controlled trials about the effects of motor imagery-based brain-computer interface training in patients with stroke were retrieved from databases (PubMed, Web of Science, Embase, Cochrane Library, CBM, CNKI, VIP, and WanFang Data) from the establishment of the databases to July 2025. Two researchers independently conducted literature screening and data extraction. The Cochrane bias risk was used to evaluate the level of evidence. Rev Man 5.4 software was used for meta-analysis. RESULTS: Eleven studies encompassing 543 stroke survivors were ultimately included. The results of the meta-analysis showed that the experimental group had better outcomes than the control group in terms of the Fugl Meyer assess...
Acta Biochimica et Biophysica Sinica•2026•DOI: 10.3724/abbs.2026098
Tumor tissues, once considered sterile, actually host diverse microbial communities that play key roles in several physiological and pathological processes, closely related to tumorigenesis and progression. Studies have demonstrated that intratumoral microbiota potentially contributes to immune regulation and significantly influences cancer treatment outcomes. Here, we aim to provide an extensive review of the conceptual framework, potential origins, spatial heterogeneity, and analytical methodologies of intratumoral microbiota, explore their carcinogenic mechanisms and potential role in tumor prognosis. In addition, we discuss current therapeutic strategies that target intratumoral microbiota and highlight the research prospects and limitations in this field, although there are some inevitable challenges.
Acta Biochimica et Biophysica Sinica•2025•DOI: 10.3724/abbs.2025048
Cervical cancer remains a leading cause of cancer-related mortality among women, with high-risk HPV-positive cases constituting 99% of instances. Despite wild-type p53 expression, its tumor-suppressive function is crippled by E6AP-mediated ubiquitination and HDAC6-driven deacetylation, resulting in rapid degradation and low steady-state levels. This study evaluates a combinatorial strategy employing the natural product withaferin A (WA) and the HDAC6 inhibitor ricolinostat (RIC) to simultaneously target p53 ubiquitination and acetylation in HeLa, SiHa, and Caski cervical cancer cells. Dose-response CCK-8 assays established that both agents inhibit proliferation in a dose-dependent manner. Combination treatment significantly reduced cell viability compared to monotherapies, with CompuSyn analysis yielding a combination index (CI) below 1, confirming synergy. Colony formation assays further demonstrated a marked decrease in clonogenic survival. Mechanistically, WA disrupted the p53-E6AP interaction, reducing p53 ubiquitination, while RIC inhibited HDAC6-mediated deacetylation, increasing p53 acetylation. The dual treatment stabilized p53, as evidenced by extended half-life in cycloheximide chase assays. These findings suggest that concurrent modulation of p53 post-translational modifications via WA and RIC offers a potent therapeutic avenue for cervical cancer, meriting further preclinical development.