Current Issue

  • Select all
    |
    CJBMB: 40 Years of Biochemistry and Molecular Biology in China Special Column of Single-cell and Spatial Omics
  • LIN Guan-Chuan, PAN Xing-Hua
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1559-1565. https://doi.org/10.13865/j.cnki.cjbmb.2025.10.0001
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Single-cell and spatial omics technologies are spearheading a profound paradigm shift in the life sciences, moving beyond ‘population averages’ to ‘single-cell resolution’ and reintegrating ‘cellular constitution’ with ‘tissue spatial architecture’, thereby dramatically advancing our understanding of biological complexity. This review provides a brief comprehensive overview of recent advancements in the field. Technologically, the evolution has progressed from single-cell transcriptomics to integrated approaches capturing multiple molecular layers simultaneously, while the emergence of transcriptome-badsed spatial omics has successfully preserved the spatial positioning of cells or microscosystem within native tissues, and further enabling spatial epigenomics and spatial-multiomics. Computationally, artificial intelligence and machine learning have become central engines, powering tools for data integration, spatial deconvolution, cellular communication and other novel foundation models, which not only tackle the challenges of massive datasets but also serve as instruments for novel biological discovery. These technological leaps have fostered significant theoretical innovations. In clinical translation, these technologies, particularly in precision oncology, demonstrate transformative potential by dissecting tumor heterogeneity, mapping the spatial architecture of the tumor immune microenvironment, and enabling disease modeling through single-cell-guided deconvolution of bulk data, offering new avenues for diagnosis, prognosis, and personalized therapy. Despite ongoing challenges in technological throughput, computational scalability, and clinical integration, the continued convergence of single-cell and spatial omics with AI promises to propel basic research towards a more mechanistic and predictive era, ultimately reshaping the future of precision medicine.
  • XIONG Ming-Fu, KONG Si-Yuan, ZHANG Yong-Sheng
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1566-1578. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1276
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    As an important tissue of the body (accounting for approximately 40% of body weight), skeletal muscle is composed of various cell types such as muscle fibers, muscle stem cells, and endothelial cells. It participates in physiological processes including movement, energy metabolism, and internal environment homeostasis through temporal and spatial specific regulation. Its development is divided into two critical stages: embryonic and postnatal periods. Abnormal development can lead to diseases such as muscular dystrophy and directly affect the yield and quality of livestock meat. In recent years, the combination of single-cell transcriptomics (scRNA-seq) and spatial omics (single-cell spatial omics technology) has provided a high-resolution research tool for analyzing the spatiotemporal dynamic regulatory network and intercellular interactions in skeletal muscle development. This article reviews the molecular mechanisms of skeletal muscle development and its application value in animal husbandry breeding, and systematically combs the research progress, analysis processes, data resources, and future directions of single-cell omics, spatial omics, and single-cell spatial omics technology in skeletal muscle development. Among them, single-cell omics can reveal the heterogeneity of skeletal muscle cells, myofiber differentiation trajectories in different livestock and poultry (such as cattle, pigs, and Tibetan chickens) through methods like pseudotime analysis and RNA velocity analysis. Furthermore, single-cell omics can identify key transcription factors (e.g., MYF5, MYOD1) and cell communication pathways (e.g., FGF7-FGFR2), and simultaneously clarify the molecular differences in myoblast differentiation timing and cell composition ratio among different breeds. Relying on technologies such as Visium and Seq-Scope, spatial omics realizes the spatial localization of gene expression in pathological models of mice, Atlantic salmon, and broiler chickens. Spatial omics also clarifies the spatial distribution laws of neuromuscular junction region-specific genes and inflammation-fibrosis cascade reactions, and makes up for the defect of losing spatial context in single-cell technology. Although there are limited direct application cases of single-cell spatial omics technology, it has already analyzed the abnormal fate of myoblasts in facioscapulohumeral muscular dystrophy through MERFISH technology. In terms of technology selection, it is necessary to consider research objectives, molecular modalities, and resolution requirements. At the same time, data analysis needs to address challenges such as data sparsity through methods like DCA denoising and RCTD cell type mapping. In addition, this article summarizes 16 muscle development-related databases including HCA and PanglaoDB. This review further discusses the potential applications of these three types of technologies in the directional regulation of myoblast fate, precise intervention in the growth cycle, improvement of microenvironment interactions, and the development of multi-omics genetic breeding models. This paper is providing a more comprehensive and detailed theoretical reference and technical support for basic research on skeletal muscle development and practical applications in the animal husbandry industry.
  • LUO Yu-Yan, LUO Xiao-Min, HUANG Jie-Ru, XU Si-Wen
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1579-1589. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1270
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Single-cell assay for transposase-accessible chromatin sequencing (scATAC-seq) is a powerful technique for studying cellular heterogeneity and gene regulatory networks, widely applied in epigenetic research. However, the complexity of data analysis workflows and high programming requirements have limited its broader adoption among non-programmer researchers. To address this issue, we developed Signac.UIO, a modular and visual scATAC-seq analysis platform based on the R Shiny framework, integrating mainstream tools such as Signac and Seurat. The platform includes ten key modules covering quality control, cell filtering, dimensionality reduction, clustering, differential analysis, cell annotation, pathway enrichment, motif analysis, and transcription factor footprinting. Through a graphical user interface, users can perform full analyses and obtain interactive visualization results. The platform’s stability and utility have been validated using a public PBMC dataset and it is currently deployed online (https://xulabgdpu.org.cn/Signac.UIO), providing an efficient and user-friendly tool for single-cell epigenomics research.
  • ZHU Xian-Pei, NIU Bin, YANG Jie-Lin
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1590-1599. https://doi.org/10.13865/j.cnki.cjbmb.2025.07.1052
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    This review aims to summarize the progress of multi-omics technologies in the study of antibiotic resistance in Cronobacter, with the goal of gaining a deep understanding of its resistance mechanisms and providing a scientific basis for the development of new treatment methods and prevention strategies. By integrating genomics, transcriptomics, proteomics, and metabolomics, the study analyzes gene variations, expression patterns, protein function changes, and metabolic pathway adjustments in Cronobacter. This includes the use of whole-genome sequencing to reveal gene variations related to antibiotic resistance, RNA-seq technology to monitor changes in gene expression patterns, proteomics to study protein expression and function, and metabolomics to analyze dynamic changes in metabolites. The research has found that factors such as biofilm formation and outer membrane proteins significantly affect the antibiotic resistance of Cronobacter. In addition, new potential influencing factors have been identified, including the expression changes of multidrug efflux pump genes, which may play a key role in enhancing antibiotic efflux and reducing intracellular antibiotic concentrations. Multi-omics technologies provide a comprehensive and in-depth perspective for the study of antibiotic resistance in Cronobacter, revealing multiple factors and potential mechanisms that affect resistance. Although some new influencing factors have been identified, their specific molecular mechanisms still require further investigation. The application prospects of multi-omics technologies are broad, and they are expected to provide important support for the development of new treatment methods and prevention strategies.
  • ZHU Xiao-Xi, WANG Cheng, YU Li-Mei
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1600-1609. https://doi.org/10.13865/j.cnki.cjbmb.2025.10.1273
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Ischemic stroke (IS) research has faced bottlenecks due to the limitations of conventional technologies in resolving cellular heterogeneity and spatiotemporal dynamics. The development of single-cell and spatial omics technologies provides revolutionary tools to break through these constraints. Single-cell omics technologies, by performing high-throughput sequencing on thousands of cells, reveal the high heterogeneity and dynamic state transitions of neurons, glial cells, immune cells, and others post-IS. For instance, microglia contain pro-inflammatory and anti-inflammatory functional subsets, while astrocytes exhibit distinct activation state spectra. Pseudotime analysis further reconstructs the fate trajectories of cells during the damage and repair processes. Spatial omics technologies, conversely, reconstruct spatial maps of gene expression through in situ capture, elucidating molecular gradients between the ischemic core, penumbra, and healthy brain regions, and enabling the analysis of critical cell-cell interaction networks. Integrating the deep phenotyping capability of single-cell sequencing with the in situ localization information from spatial omics constitutes the current core strategy. This multimodal analysis allows for precise anchoring of cell subtypes to their spatial microenvironments, revealing their distribution patterns and functions, and constructing a more accurate atlas of cell-cell communication. This significantly advances the refined dissection of IS mechanisms. This strategy has already accelerated the discovery of potential biomarkers and spatiotemporally specific therapeutic targets. Although challenges remain in sample preparation, data integration, and technical noise, future interdisciplinary collaboration, multi-omics integration, and in-depth mining with artificial intelligence promise to comprehensively transform our understanding of IS. Ultimately, it holds the potential to promote advances in its early diagnosis, precise subtyping, and the development of individualized treatment strategies.
  • LI Liu-Jia-Yu, WANG Cheng, YU Li-Mei
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1610-1621. https://doi.org/10.13865/j.cnki.cjbmb.2025.10.1268
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Mesenchymal stem cells (MSCs) hold great promise in regenerative medicine due to their multi-lineage differentiation potential and immunomodulatory properties. However, their functional heterogeneity and strong dependency on the microenvironment remain major challenges for clinical application. In recent years, the combination of single-cell transcriptome sequencing (scRNA-seq) and spatial transcriptomics sequencing (ST-seq) has provided revolutionary tools for systematically deciphering the heterogeneity, functional diversity, and microenvironmental interactions of MSCs. Using scRNA-seq, researchers have successfully resolved the functional heterogeneity of MSCs and identified key functional subpopulations, such as pro-angiogenic, immunoregulatory, and matrix-remodeling subsets. Meanwhile, ST-seq has revealed the distinct spatial distribution of MSCs within tissues and their dynamic interaction networks with the microenvironment. The integration of these two technologies has not only enabled the construction of a three-dimensional “identity-location-function” atlas of MSCs, but also uncovered spatiotemporal dynamic regulatory mechanisms of specific subpopulations during tissue repair. Looking forward, the combination of ultra-high-resolution ST-seq platforms such as Xenium, multi-omics integration, and artificial intelligence-driven analysis will shift MSCs research from descriptive studies toward precise intervention, offering new strategies for functional subpopulation screening and microenvironment reprogramming therapy. This review systematically summarizes the latest advances in scRNA-seq and ST-seq technologies in MSC research, discusses their applications in elucidating cellular heterogeneity, spatial microenvironment, and clinical translation, and provides a theoretical basis and technical guidance for precision treatment in regenerative medicine.
  • Review
  • NING Yan-Ping, CHEN Liu-Yan, ZHOU Su-Fang
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1622-1632. https://doi.org/10.13865/j.cnki.cjbmb.2025.07.1169
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Cell death is classified into programmed cell death (PCD) and non-programmed cell death (NCD). Necroptosis is a form of PCD that does not rely on caspases and is regulated by four signaling pathways: receptor-interacting protein kinase 1/3 (RIPK1-RIPK3), TIR-domain-containing adapter-inducing interferon-β(TRIF)-RIPK3, Z-DNA binding protein 1 (ZBP1)-RIPK3, and type I/II interferon receptors (IFNRs). These pathways interact to regulate the activity of core molecules such as RIPK1, RIPK3, and mixed lineage kinase domain-like protein (MLKL), thereby determining the occurrence of necroptosis. The dysregulation of these pathways can lead to the development of various diseases, including cancer. Necroptosis not only inhibits tumor occurrence and progression by promoting tumor cell death, but also creates a tumor microenvironment (TME) conducive to tumor cell growth through its pro-inflammatory properties, thereby promoting tumor growth and metastasis. Therefore, the dual role of necroptosis in cancer makes it an important research direction in tumor treatment. This article reviews the key signaling pathways of necroptosis, explores its interactions with other cell death pathways such as cell survival, apoptosis, and pyroptosis. Meanwhile, it analyzes the dual regulatory mechanisms of necroptosis in cancer progression and discusses the issue of overcoming tumor treatment resistance by modulating necroptosis. It further explores its potential therapeutic targets and application prospects, aiming to provide new intervention strategies and theoretical basis for cancer treatment.
  • YANG Shi-Ting, LIU Xue, LUO Wen-Xin
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1633-1644. https://doi.org/10.13865/j.cnki.cjbmb.2025.07.1114
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Folate receptor α (FRα), encoded by the FOLR1 gene, is overexpressed in various solid tumors but minimally expressed in normal cells, making it a prime target for anti-tumor therapy. Antibody-drug conjugates (ADCs) can accurately deliver cytotoxic agents to tumor cells, enhancing treatment specificity and efficacy. Recent years have seen remarkable progress in the development of FRα -targeted ADCs, with multiple drugs entering clinical trials and demonstrating promising anti-tumor activity and safety. This review covers the latest clinical advances in FRα -targeted ADCs. It provides a detailed introduction to the structure and function of FRα, its expression in solid tumors, and the clinical progress of FRα -targeted ADCs. It particularly focuses on the clinical trials of drugs like Mirvetuximab Soravtansine, Luveltamab Tazevibulin, and Farletuzumab Ecteribulin. These drugs have shown significant anti -tumor effects in different cancer types, and Mirvetuximab Soravtansine has received FDA accelerated approval. Despite their potential, FRα ADCs face challenges in clinical applications, such as toxicity management, biomarker definition, and clinical translation. Future research should optimize FRα ADC design, including antibody selection, linker stability, and drug load efficiency, and explore their combination with other therapies to enhance efficacy and broaden the therapeutic window. Additionally, in-depth studies on the role of FRα in the tumor microenvironment and its interaction with other signaling pathways will strengthen the theoretical basis for FRα ADC drug development. In summary, the development of FRα ADC drugs is rapidly advancing and is expected to offer new treatment options for FRα-positive cancer patients.
  • YANG Ling, ZHANG Zheng
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1645-1655. https://doi.org/10.13865/j.cnki.cjbmb.2025.08.1152
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Cardiovascular diseases (CVDs) remain one of the leading causes of morbidity and mortality worldwide. In recent years, increasing evidence has highlighted the pivotal roles of circular RNAs (circRNAs) in CVDs. Mitochondrial function, essential for cardiomyocytes to sustain energy metabolism, redox homeostasis, and calcium balance, can be modulated by circRNAs through various mechanisms. These include regulation of mitochondrial DNA (mtDNA) expression and stability, intervention in oxidative phosphorylation (OXPHOS) and reactive oxygen species (ROS) generation, control of mitochondrial calcium homeostasis, and participation in dynamic events such as fusion, fission, and mitophagy. Although the predominant model involves circRNAs acting as “miRNA sponges” in competing endogenous RNA (ceRNA) networks, more direct interactions—potentially with mitochondrial proteins, transcription, or replication factors—have yet to be fully elucidated. From a technical standpoint, current approaches to circRNA identification, functional assays, and mitochondria-specific enrichment remain suboptimal, and the majority of studies rely heavily on cell culture and animal models with limited multi-organ or disease-specific validation. Looking ahead, an integrated multi-omics framework that incorporates spatially resolved transcriptomics, RNA chemical modification profiling and protein interactome analysis will enable a systematic dissection of the circRNA-mitochondrial network, thereby opening new avenues for regulating energy metabolism in cardiomyocytes and vascular cells and for advancing the diagnosis and treatment of cardiovascular diseases.
  • ZHANG Xiao-Juan, WANG Liang-Hua
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1656-1667. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1209
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Small molecules generally refer to natural compounds with a molecular weight less than 1 kD, which have significant research value in many fields such as biological science, pharmaceutical and health care, and environmental science, etc. Aptamers, as a new type of bio-recognition element, can bind specifically to small molecules and other targets with high affinity. They are single-stranded short nucleotide sequences selected by the systematic evolution of ligands by exponential enrichment (SELEX) technology. Compared with aptamers of large molecules, aptamers of small molecules often exhibit disadvantages such as difficult screening, low affinity, and poor specificity. To solve these bottleneck problems, the article provides some strategies of screening and identification of aptamers for small molecules. Firstly, when designing the screening plan for aptamers of small molecules, this article suggests focusing on key points such as library design, SELEX methods, amplification methods, screening process monitoring methods, and aptamer sequence analysis methods, then choosing or designing appropriate strategies based on the actual situation. Secondly, the structure and affinity of aptamers directly affect their applications. The article briefly introduces methods for analyzing the secondary and tertiary structures of aptamers and six common methods for affinity determination. Finally, the article discusses some problems existing in screening and identification of aptamers for small molecules and looks forward to future development prospects. The whole article aims to provide research strategies for multiple steps of screening and identification of aptamers for small molecules and offer references for improving the efficiency of aptamer screening and identification.
  • Research Paper
  • QIU Sai-Tao, ZHAO Jun-Jun, REN Xiao-Xi, ZHANG Li-Rong, ZHOU Tai, ZHANG Jian-Liang
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1668-1677. https://doi.org/10.13865/j.cnki.cjbmb.2025.08.1159
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Parkinson’s disease (PD) is one of the most common neurodegenerative disorders. Recent evidence implicates pyroptosis as one of the pathogenic mechanisms in central nervous system disorders, although its specific mechanisms remain unclear. In this study, SH-SY5Y cells were transfected with pyroptosis-related proteins GSDME full-length (GSDME-F) or GSDME-N terminal (GSDME-N) plasmids revealed that GSDME-N significantly reduced mitochondrial membrane potential (P<0.0001). To investigate the mechanism by which GSDME mediates mitochondrial dysfunction, Western blotting analysis demonstrated that transfection with GSDME-N plasmids significantly increased BAX expression and enhanced its translocation to mitochondria in both HEK 293T and SH-SY5Y cells (P<0.05). SH-SY5Y cells treated with varying concentrations of rotenone (ROT) exhibited GSDME cleavage, elevated BAX expression (P<0.05), increased mitochondrial BAX aggregation (P<0.05), and reduced mitochondrial membrane potential (P<0.01), as confirmed by Western blotting and JC-1 staining. Concurrently, MTT assays assessing cell viability and lactate dehydrogenase (LDH) release assays indicated that ROT induced these processes prior to pyroptosis. Furthermore, in a ROT-induced mouse PD model, ROT triggered GSDME cleavage, enhanced BAX expression, caused dopaminergic neuronal damage, and induced motor deficits. In summary, this study demonstrates that GSDME-N exacerbates mitochondrial damage and increases cytotoxicity by upregulating BAX expression and facilitating its mitochondrial translocation. This study provides novel insights into the role of GSDME in PD pathogenesis and suggests potential avenues for therapeutic intervention.
  • YANG Rui, GU Bian-Li, SHI Lin-Lin, LI Shuo-Xuan, LANG Yao-Wu,
    ZUO Zhi-Xiang, GAO She-Gan
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1678-1686. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1186
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Recent studies have revealed a significant association between Porphyromonas gingivalis (P. gingivalis) infection and poor prognosis in esophageal squamous cell carcinoma (ESCC). Although certain circular RNAs (circRNA) have been shown to suppress ESCC tumorigenesis and progression, their regulatory mechanisms in P. gingivalis infection-associated ESCC remain elusive. In this study, RT-qPCR analysis demonstrated that P. gingivalis infection downregulated hsa_circ_0057552 expression in ESCC cells and tissues in a time- and dose-dependent manner. Actinomycin D assays further confirmed that P. gingivalis infection reduced the RNA stability of hsa_circ_0057552 in ESCC cells(P<0.05). Functional assays in vitro and a subcutaneous tumor xenograft model in vivo revealed that hsa_circ_0057552 overexpression significantly inhibited ESCC cell proliferation, migration, invasion, and tumor growth(P<0.05). Additionally, PCR array screening combined with RT-qPCR and Western blotting indicated that P. gingivalis infection markedly upregulated human antigen R (HuR) expression at both RNA and protein levels(P<0.05). Mechanistic investigations demonstrated that HuR knockdown significantly increased hsa_circ_0057552 expression(P<0.01), whereas hsa_circ_0057552 overexpression had no regulatory effect on HuR. Finally, si-HuR treatment reversed the inhibitory effect of P. gingivalis on hsa_circ_0057552 transcription. This study demonstrated that P. gingivalis may promote the progression of ESCC through a novel mechanism involving the regulation of HuR/hsa_circ_0057552, thereby identifying a novel therapeutic target and molecular marker for P. gingivalis-associated ESCC.
  • HUANG Lin-Yuan, GAO Jing, SUN Yi-Jin, JI Hou-Jing
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1687-1699. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1112
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    The fat mass and obesity associated gene (FTO), a crucial RNA N6-methyladenosine (m6A) demethylase, has been reported to influence the expression of glutathione peroxidase 4 (GPX4) by modulating m6A modifications. GPX4 is a key molecule inhibiting ferroptosis, and the activation of ferroptosis signaling has been demonstrated to significantly reduce lipid accumulation in both mouse primary adipocytes and high fat diet fed mice. However, the specific m6A modification sites within theGpx4 mRNA remain undefined, and the regulatory role of Gpx4 during mouse adipocyte differentiation is also unclear. Through bioinformatic analysis combined with validation by methylated RNA immunoprecipitation sequencing (MeRIP)-qPCR and single-base elongation-and ligation-based qPCR amplification method (SELECT) assays, a key m6A modification site in Gpx4 mRNA was identified at 303 bp downstream from its transcription start site. CRISPR-Cas9-mediated knockdown of Gpx4 in 3T3-L1 cells, followed by adipogenic induction, revealed that Gpx4 knockdown significantly reduced intracellular lipid droplet accumulation as assessed by Oil Red O staining (P<0.001). RT-PCR and Western blotting analyses further demonstrated significantly decreased expression of key adipogenic differentiation genes (C/ebpα, Pparγ, Lpl, Fabp4) (P<0.001). To investigate the temporal specificity of Gpx4 regulation, the GPX4 inhibitor RSL3 (100 nmol/L) was administered during different stages of adipogenic differentiation. Results showed that RSL3 treatment specifically during the mitotic clonal expansion phase significantly suppressed the expression of adipogenic genes (Fabp4, Pparγ, Adipoq) and impeded adipogenesis. In summary, this study not only identifies a key m6A modification within the mouse Gpx4 mRNA but, more importantly, reveals that GPX4 plays a critical regulatory role in 3T3-L1 adipocyte differentiation. These findings establish a link between the FTO-m6A-GPX4-ferroptosis regulatory axis and adipocyte differentiation, providing novel theoretical insights into the pathological mechanisms of obesity and identifying potential therapeutic targets.
  • YUAN Shun-Ling, DAI Sheng-Yu, LIN Wei, XU Di-Qun, LIU Yi-Ping
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1700-1710. https://doi.org/10.13865/j.cnki.cjbmb.2025.08.10093
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    This study aims to investigate the effects of aerobic exercise on neuroinflammation in AD mice and explore the mechanisms of neuroinflammation regulated by the blood-brain barrier, lipopolysaccharide (LPS) displacement, and glial cell activation. Twenty 3-month-old male APP/PS1 double transgenic mice were used, which were randomly divided into a sedentary group (SE-AD) and an aerobic exercise group (Run-AD), and 10 3-month-old male C57BL/6 mice were used as the control group (WT). The Run-AD group underwent 12 weeks of aerobic training. The results of the water maze showed that aerobic exercise improved the learning and memory capacity of AD mice (P < 0.05). The results of H&E staining and Nissl staining showed that aerobic exercise reduced necrotic cells and inflammatory cell infiltration in the cerebral cortex, as well as nuclear condensation in the CA1 and GD regions of the hippocampus (P < 0.05 , P < 0.01), and increased the area of Nissl bodies in the cerebral cortex and hippocampal CA3 and DG regions. Western blotting and ELISA results showed that aerobic exercise increased the expression of Occludin, ZO-1 and Claudin-5 proteins in the brain (P < 0.01), and decreased the levels of LPS in the brain (P<0.01). The qRT-PCR results exhibited that aerobic exercise decreased the expression of TLR4, MyD88, NF-κB, IL-1β, and TNF-α mRNA (P < 0.05, P < 0.01).The results of immunofluorescence staining revealed that aerobic exercise reduced the fluorescence area of brain IL-1β and TNF-α proteins (P < 0.05, P < 0.01), as well as the fluorescence area of Iba-1, GFAP, and TLR4 proteins in the cerebral cortex and hippocampus (P < 0.05 , P < 0.01). There was a high degree of overlap between Iba-1 and TLR4 fluorescence in the cerebral cortex, and GFAP was localized around Iba-1. In summary, aerobic exercise attenuates neuroinflammation in AD mice by protecting the blood-brain barrier, reducing the displacement of LPS, and subsequently weakening the immune activation of microglia to regulate the TLR4/MyD88/NF-κB signaling pathway to alleviate neuroinflammation.
  • XU Zi-Shuo, SHI Chao, CHEN Zhang-Xin, XUE Zhe-Yong, HUANG Li-Xin,
    CHANG Zhen-Zhan
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1711-1718. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1208
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Family with sequence similarity 3 member A (FAM3A), a novel mitochondrial protein, plays a pivotal role in hepatic glucose and lipid metabolism by enhancing ATP synthesis and secretion and modulating the ATP-P2 receptor-Akt signaling pathway. Dysregulation of FAM3A is closely associated with the pathogenesis of non-alcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM). In this study, targeting FAM3A as a therapeutic candidate, we conducted virtual screening to identify 47 small-molecule compounds with potential binding activity. Surface plasmon resonance (SPR) analysis revealed three compounds exhibiting high binding affinity to FAM3A. Further structural characterization of the FAM3A-compound complexes, combined with intermolecular interaction analysis, elucidated the binding mode of the lead compound Index 2 (taxifolin) to FAM3A at atomic resolution. These findings provide critical insights into the molecular mechanisms underlying ligand-FAM3A interactions and deliver valuable chemical scaffolds for the development of therapeutics targeting NAFLD and T2DM. This work establishes a foundation for advancing drug discovery efforts focused on FAM3A-mediated metabolic disorders.
  • YANG Yu, DONG Na, ZHANG Chi, HU Zhen-Zhen
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1719-1728. https://doi.org/10.13865/j.cnki.cjbmb.2025.09.1167
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    Microglia activation-mediated neuroinflammatory responses serve as a critical pathological basis for the development and progression of various brain diseases. The role of circular RNAs (circRNAs) in the regulation of neuroinflammation is increasingly being recognized. This study aimed to investigate the effect and molecular mechanisms of targeted inhibition of circular RNA Homeodomain Interacting Protein Kinase 3 (HIPK3) (circHIPK3) on lipopolysaccharide (LPS)-induced microglial polarization in BV2 cells. The results showed that LPS stimulation significantly induced polarization of BV2 cells towards the pro-inflammatory M1 phenotype and upregulated circHIPK3 expression (P<0.01). Engineered extracellular vesicles (EVs) with rabies viral glycoprotein (RVG) loaded with circHIPK3 siRNA (RVG-EVs-sicHIPK3) were successfully constructed. Transmission electron microscopy (TEM) revealed their typical EV morphology. nanoparticle tracking analysis (NTA) indicated a peak particle size of 70 nm. And Western blotting analysis confirmed the expression of characteristic membrane marker proteins. Treatment with RVG-EVs-sicHIPK3 significantly suppressed the LPS-induced elevation of inflammatory cytokines (TNF-α, IL-6, IL-1β) in the supernatant and reduced the expression of M1 phenotypic marker proteins (CD16 and CD86) (P<0.01). Concurrently, RVG-EVs-sicHIPK3 increased the number of mitophagosomes within cells, upregulated the ratio of the autophagy-related proteins LC3-II/LC3-I (P<0.01), and downregulated the expression of the autophagy-related protein p62 and mitochondrial-specific proteins (TOMM20 and TIMM23) (P<0.01). The mitophagy inhibitor Mdivi-1 significantly reversed the RVG-EVs-sicHIPK3-mediated downregulation of inflammatory cytokine levels, M1 marker proteins, and mitochondrial protein expression (P<0.01). This study demonstrates that inhibiting circHIPK3 reduces LPS-induced microglial polarization towards the M1 phenotype. The protective mechanism is closely associated with enhanced mitophagic flux and the promotion of damaged mitochondrial clearance.
  • Education and Teaching
  • JIN Yu-Lan, LUO Li-Jian, CHEN Xue-Qiu, WU Xiao-Feng
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1729-1736. https://doi.org/10.13865/j.cnki.cjbmb.2025.05.1056
    Abstract ( ) Download PDF ( )   Knowledge map   Save
    The Animal Molecular Biology course is a crucial and foundational course for both Animal Medicine and Animal Science majors. Apart from teaching fundamental principles of molecular biology, the course provides updated applications of these principles in the field of animal science research. Importantly, it plays a fundamental role in cultivating students’ research capabilities. With the rise of overwhelming information and their optimal utilization, the demand for integrating digital education with traditional teaching methods is increasing. Based on the five years of teaching practice, this paper summarizes four highlights of the course: the construction of teaching resource, the restructuring of teaching syllabus, the adjustment of classroom teaching hours, and the improvement of assessment methodology. It focuses on Electronic-Learning “E (E-Learning)”, offline classroom intensive teaching “C (Classroom)”, and post-class extension to construct a blended teaching model that integrates Electronic-Learning and Classroom teaching, namely the “E+C” blended teaching model. Offline classroom teaching emphasizes the combination of theory and knowledge systems, while online Electronic-Learning mainly focuses on popular science and interesting aspects to stimulate students’ interests and enthusiasm in learning. Over five years of practice, the “E+C” blended model has been proven to exert a good teaching effect. Students have reported significant gains from the course, with tightly connected and strongly complementary classroom teaching and E-Learning, which greatly aids in mastering professional knowledge. It also cultivates intrinsic motivation for learning and enhances the sense of accomplishment in acquiring knowledge, significantly improving teaching effectiveness.
  • Cover Image Introduction
  • Cover picture designer XIONG Ming-Fu
    Chinese Journal of Biochemistry and Molecular Biology. 2025, 41(11): 1737-1737.
    Abstract ( ) Download PDF ( )   Knowledge map   Save