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

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Chinese Journal of New Drugs2026

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

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.

Read Full Abstractpub_80__articleID_413

PDK4-driven metabolic reprogramming enhances mesothelial cell invasion in colorectal cancer peritoneal metastasis

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Acta Biochimica et Biophysica Sinica2026

PDK4-driven metabolic reprogramming enhances mesothelial cell invasion in colorectal cancer peritoneal metastasis

Mesothelial cells play an important role in colorectal cancer peritoneal metastasis (CRC-PM), where they support tumor growth and invasion. In this study, we investigate the molecular mechanisms by which mesothelial cells contribute to CRC metastasis. Using single-cell RNA sequencing (scRNA-seq) on tissue samples from 12 CRC patients with peritoneal metastasis, we identify PDK4 as a key gene in mesothelial cells during metastasis. The expression of PDK4 is significantly greater in mesothelial cells undergoing mesothelial-to-mesenchymal transition (MMT) compared to normal peritoneal cells, suggesting its involvement in mesothelial cell reprogramming during peritoneal metastasis. In vitro experiments show that coculturing mesothelial cells with CRC cells leads to increased PDK4 expression, which in turn enhances mesothelial cell migration and invasion. Knockdown of PDK4 reduces mesothelial cell invasion, while overexpression of PDK4 increases invasive ability, highlighting its critical role in mesothelial cell invasion. Additionally, PDK4 promotes metabolic changes, specifically increasing fatty acid oxidation (FAO), which is necessary for mesothelial cell invasion. Blocking FAO reduces the invasive ability of PDK4-overexpressing mesothelial cells, while restoring FAO in PDK4-knockdown cells rescues their invasion potential. Further analysis shows that PDK4 enhances the acetylation of β-catenin, a protein involved in cell movement, and that this modification is crucial for mesothelial cell invasion. Our results suggest that PDK4 regulates mesothelial cell invasion through β-catenin acetylation following metabolic reprogramming, offering a potential target for therapies aimed at inhibiting CRC-PM.

Read Full Abstract10.3724/abbs.2025148

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

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Chinese Journal of New Drugs2026

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

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.

Read Full Abstractpub_80__articleID_418

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

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Chinese Traditional and Herbal Drugs2025

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

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.

Read Full Abstract10.7501/j.issn.0253-2670.2025.16.20251600

Atractylenolide I mitigates Alzheimer’s disease pathology in ApoE–/– mice via ARG1/nNOS axis and lipid homeostasis regulation

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Acta Biochimica et Biophysica Sinica2026

Atractylenolide I mitigates Alzheimer’s disease pathology in ApoE–/– mice via ARG1/nNOS axis and lipid homeostasis regulation

Apolipoprotein E (ApoE) serves as a critical molecular nexus between Alzheimer’s disease (AD) and atherosclerosis, two age-associated inflammatory disorders that share vascular pathology, amyloid-beta (Aβ) deposition, and lipid dysregulation. Atractylenolide I (AI), a promising therapeutic candidate derived from Atractylodes macrocephala Koidz., exhibits multimodal bioactivities with demonstrated anti-inflammatory and neuroprotective properties. To explore its therapeutic potential against AD pathology, we use high-fat diet (HFD)-fed ApoE knockout (ApoE–/–) mice treated with or without AI for 12 weeks. Integrated bioinformatics analyses and experimental validation reveal that AI treatment markedly attenuates systemic lipid dyshomeostasis, particularly cerebral lipid deposition, suppresses neuroinflammation via downregulation of M1 macrophage polarization markers, and restores cognitive function through neuronal preservation in hippocampal regions. Mechanistically, AI orchestrates cholesterol efflux by upregulating ATP-binding cassette transporter A1 (ABCA1) and liver X receptor (LXR) expression, while concurrently modulating the abundance of arginine biosynthesis metabolites (urea, malic acid, and creatinine) to rebalance neurovascular homeostasis. Notably, western blot and RT-qPCR analyses reveal that AI differentially regulates key enzymes including arginase 1 (ARG1) and simultaneously upregulates the expression of neuronal nitric oxide synthase (nNOS). Further molecular docking and surface plasmon resonance (SPR) analyses confirm the direct binding of AI to ARG1, indicating a novel neuroprotective mechanism involving the modulation of arginine metabolism. These findings delineate the pleiotropic effects of AI against AD pathology and establish a preclinical foundation for the development of AI-based therapeutics targeting neurodegenerative-cardiovascular comorbidities.

Read Full Abstract10.3724/abbs.2026055

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

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Chinese Journal of New Drugs2026

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

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.

Read Full Abstractpub_80__articleID_430

Causal Association of Educational Attainment with Substance Use Disorders: A Mendelian Randomization Study

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Chinese Journal of New Drugs2026

Causal Association of Educational Attainment with Substance Use Disorders: A Mendelian Randomization Study

Substance use disorders (SUDs) impose a substantial global health burden, and educational attainment (EA) has been inversely associated with SUD risk in observational studies. However, the causal nature of this association remains unclear due to potential confounding and reverse causation. We conducted a two-sample Mendelian randomization (MR) study to investigate the causal effect of EA on the risk of alcohol dependence, cannabis use disorder, opioid use disorder, and other substance use disorders. Genetic instruments for EA were derived from a large genome-wide association study (GWAS) of 1.1 million individuals, and summary statistics for SUDs were obtained from the Psychiatric Genomics Consortium and other large-scale GWAS. The primary analysis used the inverse-variance weighted (IVW) method, with sensitivity analyses including weighted median, MR-Egger, and MR-PRESSO to assess pleiotropy and robustness. Genetically predicted higher EA was significantly associated with reduced risk of alcohol dependence (OR = 0.58, 95% CI: 0.49-0.69, P = 1.2×10⁻¹⁰), cannabis use disorder (OR = 0.64, 95% CI: 0.53-0.77, P = 3.4×10⁻⁶), and opioid use disorder (OR = 0.72, 95% CI: 0.58-0.89, P = 0.002). No significant association was found for other SUDs. Sensitivity analyses yielded consistent estimates, and no evidence of horizontal pleiotropy was detected. Our findings support a causal protective effect of higher educational attainment on the risk of alcohol, cannabis, and opioid use disorders. Policies aimed at improving educational outcomes may contribute to reducing the burden of substance use disorders.

Read Full Abstractpub_80__articleID_435

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

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Chinese Journal of New Drugs2026

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

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.

Read Full Abstractpub_80__articleID_432

Expression characteristics of serum exosomal microRNAs in patients with liver injury induced by anti-tuberculosis drugs

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Acta Biochimica et Biophysica Sinica2026

Expression characteristics of serum exosomal microRNAs in patients with liver injury induced by anti-tuberculosis drugs

Drug-induced liver injury (DILI) caused by anti-tuberculosis drugs is a serious clinical problem that can lead to acute liver failure and even death. Early identification of anti-tuberculosis drug-induced liver injury (TB-DILI) is crucial to avoid severe outcomes. Current diagnosis relies on lagging indicators such as serum transaminase levels, which increase only 48–72 hours after liver injury. This study is the first to systematically analyze the microRNA (miRNA) expression profile of serum exosomes in patients with TB-DILI, aiming to discover early diagnostic markers. Serum samples were collected from 12 tuberculosis patients (5 with TB-DILI, 7 with normal liver function) and 6 normal controls. Extracellular vesicles were isolated via size exclusion chromatography and characterized by transmission electron microscopy, Western blot, and NanoFCM. Small RNA sequencing identified 701 miRNAs, with 128 differentially expressed between TB-DILI and TB groups (83 upregulated, 45 downregulated). Notably, miR-122-5p was upregulated and has been shown to increase within 24 hours of isoniazid administration, earlier than ALT elevation. Target gene prediction and pathway analysis revealed enrichment in PI3K/Akt, calcium, and Wnt signaling pathways. Six core miRNAs were selected to form a TB-DILI-specific diagnostic profile. These findings suggest that serum exosomal miRNAs, particularly miR-122-5p, hold promise as early biomarkers for TB-DILI, enabling timely intervention and improved patient outcomes.

Read Full Abstract10.3724/abbs.2025242

Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis

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Acta Biochimica et Biophysica Sinica2026

Tanshinones from Salvia miltiorrhiza alleviate ulcerative colitis via reprogramming the gut microbiota-metabolite axis

The anti-inflammatory properties of the traditional herb Salvia miltiorrhiza Bunge are well-established, yet its precise mechanism of action in ulcerative colitis (UC) remains unclear. Herein, we evaluate the therapeutic potential of four major tanshinones–tanshinone IIA (Tan IIA), miltirone, neocryptotanshinone, and dihydrotanshinone I–in a murine dextran sulfate sodium (DSS)-induced colitis model. Our results show that tanshinones effectively alleviate disease severity, suppress systemic and local inflammation, and restore intestinal barrier integrity. Integrated multi-omics analysis reveals that the therapeutic efficacy originates from a comprehensive reprogramming of the gut microbiota-metabolite axis. Specifically, tanshinones reverse colitis-associated dysbiosis and rectify metabolic disturbances in linoleic acid metabolism, bile acid biosynthesis, and amino acid utilization. Correlation network analysis identifies key functional modules linking beneficial microbes (e.g., Akkermansia) to anti-inflammatory lipid mediators and associating pathobionts (e.g., Desulfovibrio) with disrupted bile acid metabolism. Notably, supplementation with Akkermansia muciniphila synergizes with Tan IIA to amplify barrier restoration and metabolic normalization. Our findings establish that tanshinones ameliorate UC through microbiota-driven metabolic reprogramming, wherein the restructured microbial community actively shapes a therapeutic metabolic output. This work elucidates a metabolite-mediated mechanism of action and positions tanshinones as promising microbiome-targeting therapeutics for inflammatory bowel disease.

Read Full Abstract10.3724/abbs.2026054

Deep Learning-Based Prediction of Drug-Induced Liver Injury Using Molecular Graph Representations

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Chinese Traditional and Herbal Drugs2026

Deep Learning-Based Prediction of Drug-Induced Liver Injury Using Molecular Graph Representations

Drug-induced liver injury (DILI) is a major cause of acute liver failure and a leading reason for drug attrition during development. Early and accurate prediction of DILI is crucial for drug safety assessment. In this study, we propose a novel deep learning framework, DILI-Graph, that leverages molecular graph representations to predict DILI risk. The model integrates graph convolutional networks (GCNs) with attention mechanisms to capture both local and global structural features of drug molecules. We trained and evaluated DILI-Graph on a comprehensive dataset of 1,200 compounds with well-annotated DILI labels. Our model achieved an area under the receiver operating characteristic curve (AUC) of 0.92, outperforming traditional machine learning methods and existing deep learning approaches. Furthermore, we performed feature importance analysis to identify key molecular substructures associated with DILI, providing interpretable insights. The proposed framework demonstrates robust performance and generalizability across external validation sets. Our findings suggest that molecular graph-based deep learning can significantly enhance DILI prediction, offering a valuable tool for preclinical drug safety screening.

Read Full Abstract10.7501/j.issn.0253-2670.2026.6.2026060

Structural and functional insights into the distinct DNA recognition mechanisms of the terminase small subunit TerS from cyanophages

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Acta Biochimica et Biophysica Sinica2026

Structural and functional insights into the distinct DNA recognition mechanisms of the terminase small subunit TerS from cyanophages

Efficient genome packaging is a critical step in the phage life cycle, directly influencing viral maturation and infectivity. In tailed phages, this process is driven by a packaging motor composed of a portal protein and a terminase complex. The terminase complex usually consists of a large subunit (TerL) and a small subunit (TerS), which cooperate to recognize, cleave, and translocate genomic DNA into the capsid. However, due to the remarkable diversity and complexity of phage packaging systems, the molecular mechanisms governing TerS-mediated DNA recognition remain poorly understood. Here, we report the 3.51 Å cryo-electron microscopy structure of the TerS from the short-tailed cyanophage Pam5, which infects the host Pseudanabaena mucicola Chao 1806. Pam5 TerS assembles into a nonameric ring with a radially symmetric spiral architecture. Biochemical assays show that Pam5 TerS recognizes the genomic DNA via a specific interaction between the N-terminal helix-turn-helix (HTH) domain of TerS and a 21-bp DNA sequence within the terS gene. In contrast, the TerS from another short-tailed cyanophage, Pam1, which infects the same host, binds to DNA in a sequence-independent manner. These findings reveal that cyanophages, even infecting the same host, could adopt two distinct DNA recognition strategies: HTH-mediated sequence-dependent or sequence-independent modes. This work provides structural and mechanistic insights into the diverse DNA-recognition strategies of TerS and advances our understanding of the evolutionary plasticity of viral genome packaging mechanisms.

Read Full Abstract10.3724/abbs.2026042

Bioinformatics classification of the MgtE Mg2+ channel and de novo protein design for the stabilization of its novel subclass

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Acta Biochimica et Biophysica Sinica2026

Bioinformatics classification of the MgtE Mg2+ channel and de novo protein design for the stabilization of its novel subclass

MgtE channels play crucial roles in Mg2+ homeostasis and are implicated in bacterial survival under antibiotic exposure. Previous structural and biophysical studies have focused predominantly on Thermus thermophilus MgtE, leaving the structural and mechanistic diversity of MgtE family proteins largely unexplored. In this study, via a genome mining approach, we identify diverse MgtE homologs, including a novel subclass termed the “mini-N type”, which lacks the canonical cytoplasmic N and CBS domains but possesses a unique small N-like domain. Despite extensive expression screening, mini-N-type homologs cannot be stably purified. To address this issue, we design a series of de novo proteins and determine their crystal structures. A selected de novo protein is fused to a mini-N-type MgtE, enabling successful purification and preliminary cryo-EM imaging. Our findings demonstrate that de novo-designed protein fusions serve as powerful tools for stabilizing and purifying otherwise unstable membrane proteins, opening new avenues for structural and functional studies of otherwise inaccessible membrane proteins.

Read Full Abstract10.3724/abbs.2025224

Caught the ‘Catch’ of midnolin: structural basis for broad substrate specificity in ubiquitin-independent proteasomal degradation

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Acta Biochimica et Biophysica Sinica2026

Caught the ‘Catch’ of midnolin: structural basis for broad substrate specificity in ubiquitin-independent proteasomal degradation

Protein homeostasis is fundamental to cellular decisions, and its dysregulation drives numerous pathologies. The ubiquitin-independent proteasomal degradation pathway mediated by midnolin (MIDN) has emerged as a distinct mechanism for regulating nuclear protein turnover. In the current study, Zhong et al. provide a comprehensive structural and biochemical analysis of the MIDN Catch domain bound to IRF4-derived peptides, substantially advancing our understanding of MIDN substrate recognition. By solving multiple crystal structures of the Catch-IRF4 complex, the authors demonstrate that MIDN recognizes substrates through a conserved β-strand insertion mechanism at the interface of the Catch1 and Catch2 subdomains. A major conceptual advance is the identification of a minimal and generalizable recognition principle centered on two highly conserved positions within the substrate motif, forming an 'F-G zipper' that constitutes the dominant energetic determinant for binding. In contrast, flanking residues display remarkable tolerance to substitution, occupying large and plastic hydrophobic pockets in the Catch domain. This architectural flexibility provides a direct molecular explanation for how MIDN can accommodate a wide spectrum of substrates while preserving selectivity. The authors derive a concise consensus recognition motif (G/S-x-F/Y) embedded within an unstructured or loop region, offering a predictive framework for identifying additional MIDN targets. Importantly, this work bridges a critical gap between previous cryo-EM studies describing MIDN-proteasome engagement and earlier substrate-specific structural analyses. Overall, this study represents a significant advance in the field of proteostasis by revealing how a ubiquitin-independent adaptor achieves broad substrate specificity through a simple yet robust structural principle, with important implications for immune regulation, neurodegeneration, and cancer biology.

Read Full Abstract10.3724/abbs.2026006

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

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Acta Biochimica et Biophysica Sinica2026

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

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.

Read Full Abstract10.3724/abbs.2026002

Mixed Fungal Polysaccharides Enhance Intestinal Health, Antioxidant Capacity, and Microbiota Diversity in Broiler Chickens

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Acta Biochimica et Biophysica Sinica2026

Mixed Fungal Polysaccharides Enhance Intestinal Health, Antioxidant Capacity, and Microbiota Diversity in Broiler Chickens

Poultry production faces escalating challenges from intensive farming practices, where stressors disrupt intestinal integrity, microbiota balance, and antioxidant defenses, leading to economic losses. Although antibiotics have historically mitigated such issues, growing restrictions due to antimicrobial resistance necessitate natural alternatives. Fungal polysaccharides (FP), notably lentinan (LNT) from Lentinula edodes and polysaccharide from Ganoderma lucidum (GLP), are promising candidates owing to their immunomodulatory, antioxidant, and prebiotic properties. However, existing research focuses predominantly on individual FP, neglecting potential synergies in blended formulations. We hypothesized that mixed FP synergistically enhance intestinal health by simultaneously improving nutrient absorption, activating antioxidant pathways, and stabilizing microbial ecosystems. To investigate, 240 one-day-old Arbor Acres male broilers were randomly assigned to control (0 mg/kg FP) and treatment groups receiving 200, 400, or 600 mg/kg mixed FP (1:1 ratio of GLP and LNT). On day 42, intestinal segments were collected for morphological analysis, antioxidant enzyme activities, gene expression, and cecal microbiota composition. Results showed that 400 mg/kg FP significantly increased villus height and VH/CD ratio across all intestinal segments while reducing crypt depth, indicating enhanced nutrient absorption. Antioxidant enzyme activities (T-AOC, T-SOD, GSH-Px) were elevated, and mRNA expression of HO-1, NQO1, CAT, and Nrf2 was upregulated, with Keap1 downregulated, suggesting activation of the Keap1-Nrf2 pathway. Microbiota analysis revealed increased alpha diversity (Shannon and Simpson indices) and altered composition, with elevated abundances of beneficial genera such as Butyricimonas and Alistipes, and increased Verrucomicrobiota phylum. These findings demonstrate that mixed FP supplementation at 400 mg/kg improves intestinal health, antioxidant capacity, and microbiota diversity in broilers, offering a natural alternative to antibiotics.

Read Full Abstract10.3724/abbs.2025222

Glycolysis Reprogramming Predicts Poor Prognosis and Drives Therapy Resistance via CLN6 in Lethal Prostate Cancer

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Acta Biochimica et Biophysica Sinica2026

Glycolysis Reprogramming Predicts Poor Prognosis and Drives Therapy Resistance via CLN6 in Lethal Prostate Cancer

Lethal prostate cancer is marked by tumor heterogeneity and resistance to androgen receptor signaling inhibitors (ARSIs). In this study, we identify glycolysis as a driver of disease progression and therapy resistance. Using single-sample gene set enrichment analysis (ssGSEA) on the SU2C cohort, we demonstrate that elevated glycolysis activity is associated with poor progression-free and overall survival. The glycolysis-based prognostic score (GLY score) is derived from the HALLMARK_GLYCOLYSIS gene set, which includes CLN6, SDHC, B4GALT2, RPE, NANP, and KIF20A, via LASSO-Cox regression. The GLY score effectively stratifies risk in the SU2C and WDCT cohorts, with higher scores predicting worse outcomes and increased SYNE1 mutation frequency. Pan-cancer analysis across TCGA datasets confirms its prognostic value. In vitro, enzalutamide-resistant prostate cancer cell lines exhibit heightened glycolysis, and 2-DG inhibition reverses this effect, restoring drug sensitivity. CLN6 knockdown reduces glycolytic activity and cell proliferation. The GLY score offers robust prognostic value, and CLN6 represents a promising therapeutic target for precision medicine in lethal prostate cancer.

Read Full Abstract10.3724/abbs.2025257

Total flavonoids of litchi seed attenuates cellular senescence by inhibiting the production of SASP through p65 suppression and ameliorates pulmonary fibrosis

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Acta Biochimica et Biophysica Sinica2026

Total flavonoids of litchi seed attenuates cellular senescence by inhibiting the production of SASP through p65 suppression and ameliorates pulmonary fibrosis

Anti-aging foods not only benefit elderly individuals but also drive the development of safe and effective natural drugs. Here, we report that the addition of total flavonoids of litchi seed (TFL) delays replicative senescence and stress-induced senescence. TFL alleviates the senescence-associated secretory phenotype (SASP) and reduces the degree of DNA damage caused by bleomycin (BLM). TFL also counteracts stress-induced pulmonary senescence and fibrosis. TFL reduces the protein level of p21 in mouse lung and alleviates pulmonary fibrosis. Transcriptome profiling further reveals that TFL plays a key role in its anti-aging mechanism by inhibiting the SASP. Mechanistically, TFL suppresses p65 protein expression, thereby inhibiting IL-1α and IL-1β and delaying cellular senescence. Gut microbiome analysis reveals that the abundance and functions of the mouse gut microbiome change after BLM exposure and that TFL treatment reverses these changes. Overall, we provide a theoretical basis for the future application of TFL as a potential anti-aging product.

Read Full Abstract10.3724/abbs.2025206

The effect of liver-specific ketohexokinase deletion on the intestinal-liver-kidney axis in high-fructose-induced metabolic syndrome mice

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Acta Biochimica et Biophysica Sinica2026

The effect of liver-specific ketohexokinase deletion on the intestinal-liver-kidney axis in high-fructose-induced metabolic syndrome mice

The liver is a crucial site for fructose uptake and metabolism, a function intricately linked to fructose-associated pathologies. This study examines the role of hepatic ketohexokinase (KHK) in metabolic syndrome induced solely by high-fructose intake. Liver-specific Khk-deficient mice are generated and fed with a 20% fructose solution for 3 months, after which the features of metabolic syndrome are examined. Compared with fructose-fed floxed controls, fructose-fed liver-specific Khk-deficient mice present alleviated liver injury and hepatic steatosis, along with lower triglyceride levels in the plasma and liver, plasma aspartate transaminase and alanine transaminase levels, and mRNA levels of genes related to triglyceride and fatty acid synthesis. Liver-specific Khk deficiency also leads to lower uric acid levels in the plasma and urine, as well as xanthine oxidase activity and Glut9 mRNA levels in the liver and kidneys of fructose-fed mice. Although intestinal villus length and epithelial barrier integrity remain unaffected, the deletion of liver Khk significantly reduces fructose-stimulated KHK, Glut2, Glut5, and aldolase B expression in the intestine and kidneys, suggesting inhibited fructose absorption and metabolism in these tissues. In the adipose tissue, fructose-induced increases in adipocyte size and tumor necrosis factor-α and interleukin-6 mRNA levels are blocked by liver-specific Khk deficiency, indicating improved remodeling of adipose tissue and reduced inflammation in adipocytes. Overall, liver-specific Khk deletion is sufficient to protect against metabolic syndrome induced by excessive fructose intake. Our findings underscore the critical role of liver KHK-mediated fructose metabolism in driving the physiological and pathological consequences associated with fructose consumption along the intestinal-liver-kidney axis.

Read Full Abstract10.3724/abbs.2025191

Small Chemical Molecule CPP Promotes Angiogenesis in Surgically Created Severe Lower Limb Ischemia and Diabetes-Induced Limb Vascular Reduction Models

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Acta Biochimica et Biophysica Sinica2026

Small Chemical Molecule CPP Promotes Angiogenesis in Surgically Created Severe Lower Limb Ischemia and Diabetes-Induced Limb Vascular Reduction Models

Peripheral artery disease (PAD) often progresses to chronic limb-threatening ischemia (CLTI), leading to severe limb dysfunction and amputation. Angiogenic therapies using small molecules offer advantages over cell-based approaches. Here, we investigated the in vivo angiogenic effects of CPP, a small chemical molecule previously shown to induce differentiation of human dermal fibroblasts into vascular endothelial cells via the PHD2/HIF1α/HEY1 pathway. In a mouse model of critical limb ischemia (CLI), subcutaneous multipoint injections of CPP (1 or 10 mg/kg/day) for 14 days significantly enhanced blood perfusion in ischemic limbs by day 7, with the 1 mg/kg dose increasing capillary density in skin and muscle by day 14. High-dose CPP showed no organ toxicity. In diabetic db/db mice, intraperitoneal CPP (1 or 5 mg/kg/day) for 30 days restored capillary density in skin and gastrocnemius muscle, counteracting diabetes-induced vascular rarefaction. These findings demonstrate that CPP promotes in situ angiogenesis and perfusion recovery in ischemic and diabetic conditions, highlighting its potential as a therapeutic agent for PAD.

Read Full Abstract10.3724/abbs.2026039

SinoBioData ResearchActa Biochimica et Biophysica Sinica

Acta Biochimica et Biophysica Sinica2026

Fibroblast growth factor 13 deficiency attenuates doxorubicin-induced cardiotoxicity by regulating Parkin-mediated myocardial injury

The clinical use of doxorubicin (DOX) as a chemotherapeutic agent is limited by its cardiotoxic effects. Fibroblast growth factor (FGF) isoform 13, a distinct type of FGF, has been increasingly recognized as an important regulator of cardiovascular disease. However, its role in doxorubicin-induced cardiotoxicity remains unknown. Therefore, the objective of this study is to investigate the role and mechanism of FGF13 in doxorubicin-induced cardiac injury. C57BL/6 mice are used to establish Dox-induced cardiotoxicity models. The results reveal that mouse weight, cardiomyocyte cross-sectional area, ejection fraction and fractional shortening are decreased in the DOX group. In contrast, Fgf13 deficiency mitigates doxorubicin-mediated cardiotoxicity, as indicated by increased mouse weight, cardiomyocyte cross-sectional area, ejection fraction and fractional shortening. Mechanistically, the protein expressions of bax and cleaved caspase 3 are elevated in the DOX-treated group, along with decreased JC-1 fluorescence intensity and bcl-2 expression, whereas Fgf13 knockout prevents these alterations. In addition, Parkin, but not p53, interacts with FGF13 and is upregulated in response to Fgf13 deficiency in a mouse model of doxorubicin-induced cardiotoxicity. Overall, Fgf13 knockout attenuates doxorubicin-induced cardiomyocyte apoptosis and mitochondrial damage through the modulation of Parkin, indicating that FGF13 may serve as a promising therapeutic target for DOX-induced cardiotoxicity.

Read Full Abstract10.3724/abbs.2025223

A protein-RNA complex orchestrated by EMB1006, EMB1270, EMB976, and CFM2 facilitates clpP1 intron 2 splicing in Arabidopsis chloroplasts

Graphical AbstractVerified

Acta Biochimica et Biophysica Sinica2026

A protein-RNA complex orchestrated by EMB1006, EMB1270, EMB976, and CFM2 facilitates clpP1 intron 2 splicing in Arabidopsis chloroplasts

In Arabidopsis, the PPR proteins EMB1006, EMB1270, and EMB976 are all essential for the splicing of plastid clpP1 intron 2 (clpP1.2), although each also targets other distinct RNAs. The precise mechanism underlying their coordinated action in clpP1.2 splicing remains unclear. In this study, RNA electrophoretic mobility shift assays, guided by PPR code prediction, confirm that EMB1006 specifically binds to a sequence near the 3′ end of clpP1 exon 2. Additionally, immunoprecipitation coupled with mass spectrometry reveals that EMB1006 forms a complex with EMB1270, EMB976, and CFM2. Direct interactions between EMB1006 and EMB1270 or CFM2 are further supported by yeast two-hybrid (Y2H) and semi-in vivo pull-down assays. However, no direct interactions between EMB976 and EMB1006, CFM2 or EMB1270 are detected by Y2H. Based on these findings and previous evidence that EMB1270 binds to clpP1 intron 2 and interacts with CFM2, we propose a model in which EMB1006 and EMB1270 bind to distinct sites on clpP1 pre-mRNA. Together with CFM2 and possible indirect association with EMB976, they assemble into a protein-RNA complex that facilitates the splicing of clpP1.2 in chloroplasts.

Read Full Abstract10.3724/abbs.2026076

SinoBioData ResearchActa Biochimica et Biophysica Sinica

Acta Biochimica et Biophysica Sinica2026

Metabolic Reprogramming—The Nexus of Cellular Adaptations, Organ Crosstalk, and Therapeutic Innovations in Human Diseases

For decades, cellular metabolism was viewed as a static network of biochemical pathways designed solely to produce ATP and fulfill basic energy needs. Classical pathophysiology frequently attributes systemic disorders, including cardiovascular disease, oncogenesis and tissue fibrosis, to structural defects, hormonal dysregulations or localized inflammation. However, advanced multi-omics frameworks have driven a paradigm shift, with metabolic reprogramming being recognized not merely as a passive consequence of disease but also as a primary driver of initiation, progression, and therapeutic resistance across human pathologies. This Special Issue, titled “Metabolic Reprogramming,” brings together 17 comprehensive studies alongside 3 New Phenomena exploring these transformations. The contributions span four interrelated thematic areas: (1) systemic cardiometabolic and gestational syndromes; (2) acute and chronic organ injury; (3) oncological metabolic dependencies; and (4) systemic organ-axis interdependencies. By integrating transcriptomics, metabolomics, single-cell deconvolution, and targeted biochemical analyses, these studies elucidate the precise molecular mechanisms governing metabolic remodeling. Key findings include the role of tissue-specific metabolic reprogramming in cardiometabolic syndrome, the impact of pregnancy-induced skeletal muscle reprogramming on gestational diabetes, the cardioprotective mechanisms of Levosimendan via Nrf2 in septic cardiomyopathy, the protective role of SBK3 in cardiac hypertrophy, the SENP1-DDX17 axis in carfilzomib cardiotoxicity, FGF13 as a therapeutic target in doxorubicin cardiotoxicity, and the beneficial effects of aminoguanidine in diabetic vasculopathy. These insights underscore the potential of targeting metabolic pathways for innovative therapeutic strategies.

Read Full Abstract10.3724/abbs.2026110

A Novel Biomarker SNHG11 Promotes Tumor Progression and Oxidative Phosphorylation in Clear Cell Renal Cell Carcinoma

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Acta Biochimica et Biophysica Sinica2026

A Novel Biomarker SNHG11 Promotes Tumor Progression and Oxidative Phosphorylation in Clear Cell Renal Cell Carcinoma

Kidney renal clear cell carcinoma (KIRC) is the most common and aggressive subtype of renal cell carcinoma and is characterized by poor prognosis and high molecular heterogeneity. Long noncoding RNAs (lncRNAs) have emerged as crucial regulators in cancer, yet the functional role of SNHG11 in KIRC remains unclear. In this study, we perform integrated multiomics analysis using data from the TCGA and ICGC cohorts and reveal that SNHG11, a methylation-associated lncRNA, is significantly correlated with poor clinical outcomes. In vitro and in vivo assays demonstrate that SNHG11 promotes tumor proliferation and progression. Mechanistically, SNHG11 enhances oxidative phosphorylation, as evidenced by increased ATP production, disrupted mitochondrial membrane potential, and altered NAD+/NADH ratios. Furthermore, SNHG11 expression is associated with somatic mutation patterns, particularly those involving BAP1 and PBRM1, indicating potential crosstalk between epigenetic regulation and genetic alterations. These findings reveal that SNHG11 is a novel biomarker in KIRC and a potential therapeutic target.

Read Full Abstract10.3724/abbs.2025253