Cells最新文献

{"title":"Loss of <i>dmrt2a</i> Alters Hepatic LC-PUFA Composition and Lipid Homeostasis in Zebrafish.","authors":"Mingxi Hou, Donghao Li, Yaqun Zhang, Hengde Li","doi":"10.3390/cells15191763","DOIUrl":"10.3390/cells15191763","url":null,"abstract":"<p><p>Long-chain polyunsaturated fatty acids (LC-PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are essential nutrients for human health, and fish and aquatic products are the primary dietary sources of these bioactive lipids. The endogenous capacity of teleosts to synthesize LC-PUFAs directly determines their nutritional value for human consumers. However, the genetic regulators governing this biosynthetic pathway remain largely unexplored. Here, we show that targeted disruption of <i>dmrt2a</i>, a transcription factor gene, in zebrafish (<i>Danio rerio</i>) via CRISPR/Cas9, alters hepatic LC-PUFA composition and lipid homeostasis. Homozygous <i>dmrt2a</i>^-/- mutants exhibited significantly reduced molar percentages of EPA (C20:5n-3) and DHA (C22:6n-3) in the liver, accompanied by the accumulation of their precursors, C18:2n-6 and C18:3n-3. In addition, the mutants developed a hepatic lipid metabolic disorder characterized by pathological accumulation of lipid droplets and elevated triglyceride levels, thereby providing a novel zebrafish model for research on hepatic steatosis. Transcriptomic profiling revealed that differentially expressed genes between <i>dmrt2a</i>^-/- mutant and wild-type livers were significantly enriched in fatty acid biosynthesis and metabolic pathways. Notably, an LC-PUFA-enriched diet partially rescued the aberrant hepatic lipid phenotype. To our knowledge, this is the first study in any fish species to link a DMRT-family transcription factor to hepatic LC-PUFA composition and lipid homeostasis, suggesting <i>dmrt2a</i> as a potential target for genetic breeding to improve the nutritional quality of aquaculture products.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663920/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"BAP31 Facilitates TGF-β Trafficking and Secretion and Promotes Dendritic Cell Dysfunction in Cervical Cancer.","authors":"Lin Guo, Yuanli He, Feiming Hu, Yuanjie Sun, Yajie Zhang, Junyi Ren, Ren Zheng, Junqi Zhang, Yubo Sun, Sirui Cai, Yueyue Wang, Kun Yang, Chenchen Hu, Shuya Yang","doi":"10.3390/cells15191765","DOIUrl":"10.3390/cells15191765","url":null,"abstract":"<p><p>Cervical cancer remains one of the major gynecological malignancies worldwide, with tumor immune evasion playing a critical role in disease progression. Although accumulating evidence has implicated BAP31 in tumor progression and immune regulation, its role in immune evasion in cervical cancer remains poorly understood. In this study, we found that BAP31 was significantly upregulated in cervical cancer tissues and that elevated BAP31 expression was associated with poor patient prognosis. Functional assays demonstrated that BAP31 silencing restored the immune activity of dendritic cells. Mechanistically, BAP31 was found to regulate TGF-β at the post-transcriptional level and to facilitate its transport from the endoplasmic reticulum to the Golgi apparatus through an interaction involving the Asn-381 residue, thereby affecting its intracellular maturation and extracellular secretion. Additional functional analyses showed that exogenous TGF-β impaired dendritic cell maturation and migration while enhancing phagocytic activity. Collectively, these findings indicate that BAP31 regulation of TGF-β contributes to dendritic cell dysfunction and the establishment of an immunosuppressive microenvironment in cervical cancer.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663929/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redox Storm in the Tumor Microenvironment (ΤΜΕ): Multifaceted Redox Injury and Immunometabolic Reprogramming Induced by Immune Checkpoint Blockade in B16F10 Melanoma: An Ultrastructural Study of the Peritumoral Interface.","authors":"Vasileios Alexandros Karakousis, Antonia Sioga, Ioannis S Vizirianakis, Isaak Kesisoglou, Christophoros S Kosmidis, Leonidas Pavlidis, Theodora Papamitsou","doi":"10.3390/cells15191760","DOIUrl":"10.3390/cells15191760","url":null,"abstract":"<p><p>Immune checkpoint blockade (ICB) has revolutionized melanoma treatment, yet the in vivo ultrastructural consequences within the tumor microenvironment (TME) remain poorly characterized. This study investigates the morphological alterations induced by ICB at the peritumoral interface through a \"redox storm\" paradigm. B16F10 melanoma-bearing mice were treated with anti-CTLA-4, anti-PD-1, or their combination, and evaluated by transmission electron microscopy (TEM) at Days 20, 30, and 40; quantitative morphometric analyses were performed for comparative purposes. This design enabled the assessment of ultrastructural changes from initial immune activation to late-stage remodeling, linking early cytotoxic events with subsequent stromal adaptations. TEM provided evidence of a sequential redox cascade characterized by lymphocyte reactivation, mitochondrial cristolysis, lipid droplet accumulation, foamy macrophage-like cells, efferocytosis-driven M2-like polarization, and metabolic plasticity in surviving tumor cells. Specifically, combination therapy was associated with marked cytolysis and extensive stromal remodeling, while anti-PD-1 appeared to promote prominent cholesterol crystal formation and lipotoxicity. Morphometric analyses supported these qualitative findings, indicating significant alterations in lipid droplet area and cell death area across treatment groups. This ultrastructural dissection provides morphological evidence for the \"redox storm\" and offers a framework to understand ICB efficacy, resistance, and dynamic TME remodeling, ultimately providing a basis for targeted combination strategies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664297/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Placental Insulin-like Growth Factor Signaling and Neurodevelopment: Emerging Evidence from the Placenta-Brain Axis.","authors":"Annemarie J Carver, Eleanor G Williamson, Hanna E Stevens","doi":"10.3390/cells15191759","DOIUrl":"10.3390/cells15191759","url":null,"abstract":"<p><p>The field of neuroplacentology is a growing area that focuses on the influence of placental function on brain development. This field has expanded our understanding of the placenta's crucial role in proper neurodevelopment as well as placental anomalies that increase the risk of adverse neurodevelopmental outcomes. Neuroplacentology studies have revealed distinct roles of placentally provided hormones and nutrients in neurodevelopment whose disruption by perinatal problems, including inflammation, can increase the risk of neurodevelopmental disorders such as autism spectrum disorder and ADHD. Placental insulin-like growth factor signaling significantly influences brain growth in animal model studies and is tightly linked with human neurodevelopmental outcomes. Insulin-like growth factor signaling is well-established as a regulator of placental function and is fundamental in fetal brain cell developmental processes and plays a role in inflammation. Placental insulin-like growth factor signaling underlies the placental production and delivery of hormones and nutrients that are necessary for fetal neural cell proliferation, differentiation, and growth. It is especially important to study this pathway in the placenta due to aberrant insulin-like growth factor signaling found in conditions such as preterm birth, fetal growth restriction, gestational diabetes, and obesity. All these conditions are linked to a greater risk for neurodevelopmental disorders, neuroinflammation, and other anomalies. This research subfield has also revealed sex differences in the insulin-like growth factor signaling pathway that will contribute to understanding the etiologies of these conditions. This area of study has and will continue to identify specific mechanisms, many currently in model systems, which could eventually be leveraged in preventative and interventive care to improve neurodevelopmental outcomes.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664104/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correlative and Live-Cell Imaging of S100B-Promoter-Associated Interstitial Cells from the Cardiac Sinoatrial Node and Valves.","authors":"Dmitry B Zorov, Miguel Calvo-Rubio, Robert E Monticone, Bruce D Ziman, Richard Telljohann, Georgiana Luisa Baca, Khalid Chakir, Valeriya B Vays, Irina M Vangeli, Lora E Bakeeva, Ljubava D Zorova, Rostislav Bychkov, Edward G Lakatta","doi":"10.3390/cells15191762","DOIUrl":"10.3390/cells15191762","url":null,"abstract":"<p><p>Cardiac pacemaker and valve cells operate within a heterogeneous interstitial environment, but the identities and observable behaviors of many constituent cells remain incompletely defined. We integrated complementary imaging observations from a single experimental platform into an exploratory analysis of cultured cells isolated from the adult mouse sinoatrial node (SAN) and atrioventricular valves of S100B-EGFP reporter mice. Cellular morphology, endogenous NAD(P)H fluorescence, tetramethylrhodamine methyl ester (TMRM) fluorescence, correlative light and electron microscopy (CLEM), time-lapse imaging, transmission electron microscopy (TEM), and 5-ethynyl-2'-deoxyuridine (EdU) labeling were used to describe selected reporter-positive and reporter-negative cells. S100B-promoter-associated EGFP+ cells displayed heterogeneous forms, including cells with small bodies and long processes. In representative fields, EGFP+ cells showed greater NAD(P)H autofluorescence intensity and lower TMRM signal than adjacent EGFP- cells. CLEM related selected fluorescence phenotypes to ultrastructure in the same cells and documented mitochondrial, vesicular, nuclear, and membrane-associated profiles. One live sequence captured movement of a TMRM-positive, mitochondrion-like structure through a thin intercellular bridge toward an EGFP- cell, followed by bridge disassembly. Additional images showed mitochondrial and vesicular profiles near cell surfaces or in extracellularly situated regions, elongated NAD(P)H-bright structures, reporter-positive cytoplasmic fragments, nuclear size heterogeneity, a narrow connection between nuclear profiles, and unequal EdU labeling among nuclear fragments. These findings are descriptive and hypothesis-generating. They do not establish definitive cell identity, phenotype prevalence, active or selective secretion, tunneling-nanotube identity, mitochondrial metabolic competence, regulated nuclear remodeling, recipient-cell uptake, or physiological consequence. The study provides an integrated morphological framework and a set of candidate events for future quantitative investigation of S100B-associated cardiac interstitial-cell biology.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13663954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"OVO-like Proteins in Cancer, Immunity, and Inflammation.","authors":"Shuxian Huang, Genjian Hu, Hao Lan, Jinfeng Gan","doi":"10.3390/cells15191755","DOIUrl":"10.3390/cells15191755","url":null,"abstract":"<p><p>The OVO-like (OVOL) proteins OVOL1-3 are evolutionarily conserved C2H2 zinc-finger transcription factors. Initially identified in <i>Drosophila</i> as regulators of germline development, these proteins have since been found to be key determinants of epithelial lineage and differentiation in mammals. Increasing evidence implicates OVOL proteins in human disease, particularly cancer, where they participate in diverse processes including metastasis, metabolic regulation, immunity, and inflammation modulation. In this review, current advances in OVOL-related research are summarized. First, the roles of OVOL proteins in regulating epithelial-mesenchymal transition (EMT), cancer metastasis, and cellular plasticity are addressed. The discussion then extends to emerging evidence for their involvement in metabolic reprogramming, immunity, and inflammation. Finally, open questions and future research directions are discussed.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664146/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191691","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optimized Epitope-Flanking Sequences Enhance Antigen Presentation and T-Cell Responses Following mRNA Vaccination.","authors":"Marie-Pierre Hardy, Gabriel Ouellet-Lavallée, Catherine Thériault, Chantal Durette, Krystel Vincent, Robin Minati, Isabelle Caron, Assya Trofimov, Joel Lanoix, Jean-Philippe Laverdure, Pierre Thibault, Claude Perreault","doi":"10.3390/cells15191753","DOIUrl":"10.3390/cells15191753","url":null,"abstract":"<p><p>mRNA vaccines can encode multiple tumor antigens whose presentation ultimately depends on adequate intracellular processing. To evaluate the potential impact of epitope-flanking sequences, we compared the immunogenicity of two mRNA vaccines in the MC38 mouse model. Both vaccines coded for the same tumor-specific antigens (TSAs). The only difference between the two vaccines was the identity of the epitope-flanking amino acids. The vaccine encoding TSAs bordered by optimized flanking sequences (TSA-Opti) cleared established tumors and elicited robust CD8⁺ T-cell responses. In contrast, the vaccine encoding the same TSAs surrounded by natural flanking sequences (TSA-Nat) induced weaker responses and incomplete protection against tumor growth. Quantitative immunopeptidomics showed that TSA-Opti increased antigen presentation levels, providing a mechanistic link between flanking-sequence design and the enhanced magnitude, clonal diversity, and functionality of TSA-specific CD8+ T cells. TSA-Opti further promoted durable memory, conferring long-term protection against tumor rechallenge. These results identify epitope-flanking sequences as tunable design elements that control peptide-MHC I density and thereby shape the magnitude, clonal diversity, tissue localization, and durability of antitumor CD8⁺ T-cell immunity.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664092/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191742","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Damage-Associated Molecular Patterns and Trained Immunity of Monocyte-Macrophage Populations in Osteoarthritis: Potential Molecular Links and Therapeutic Opportunities.","authors":"Jian Zhang, Bingbing Chen, Yundong Xu, Heguo Yan, Niqin Xiao, Jing Xie, Zhaohu Xie, Zhaofu Li","doi":"10.3390/cells15191756","DOIUrl":"10.3390/cells15191756","url":null,"abstract":"<p><p>Osteoarthritis (OA) is now widely discussed as a whole-joint immunometabolic disease involving cartilage, synovium, and subchondral bone, rather than as cartilage degeneration driven only by mechanical stress. Tissue injury, cell death, mitochondrial dysfunction, and extracellular matrix degradation can lead to the persistent release of damage-associated molecular patterns (DAMPs), which activate innate immune responses through pattern recognition receptors (PRRs). A key unresolved issue is why inflammation can persist or recur when there is no continuous external stimulus. Trained immunity provides an emerging framework for approaching this problem, with initial direct evidence now available in circulating monocytes from knee OA but broader validation still lacking. Following an initial stimulus and a subsequent resting interval, monocytes and macrophages may retain epigenetic and metabolic alterations that modify their responses to later homologous or heterologous challenges. This review summarizes the sources of DAMPs and their recognition mechanisms in the OA microenvironment, with particular attention to their potential links with trained immunity in monocyte-macrophage populations. We discuss PRR-mediated changes in chromatin accessibility, histone modifications, DNA methylation, and non-coding RNA regulation, as well as immunometabolic events such as enhanced glycolysis, tricarboxylic acid cycle remodeling, mitochondrial dysfunction, and accumulation of key metabolites. We also examine how monocyte-macrophage populations with persistent hyperresponsiveness after stimulus withdrawal and restimulation may contribute to persistent synovitis, cartilage matrix degradation, and abnormal subchondral bone remodeling. Finally, we summarize therapeutic opportunities potentially relevant to the proposed links between DAMP signaling and trained immunity. Recent evidence that high-mobility group box 1 (HMGB1) primes a trained phenotype in circulating monocytes provides initial direct support for DAMP-associated trained immunity in knee OA. However, its generalizability across independent cohorts, other DAMP classes, myeloid-cell compartments, disease stages, and OA phenotypes remains to be established.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191497","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging Technologies in Cardiovascular Disease Modeling: Bridging Basic Science and Clinical Translation.","authors":"Ramcharan Singh Angom, Sophie K Ashbrook, Carter Magnano, Riya Kar, Anya Dorairaj, Hari Krishnareddy Rachamala, Debabrata Mukhopadhyay","doi":"10.3390/cells15191754","DOIUrl":"10.3390/cells15191754","url":null,"abstract":"<p><p>Cardiovascular diseases (CVDs) remain the leading cause of death worldwide, yet therapeutic development is limited by experimental models that incompletely recapitulate human physiology, disease heterogeneity, and treatment responses. Emerging human-relevant models, including patient-derived induced pluripotent stem cells, cardiac organoids, engineered tissues, organ-on-chip systems, genome editing, multi-omics, and computational approaches, are improving the ability to investigate cardiovascular disease mechanisms and therapeutic responses. In this review, we critically compare these technologies with respect to physiological relevance, reproducibility, scalability, throughput, and translational potential. We highlight their applications in disease modeling, drug discovery, toxicity assessment, and precision medicine while examining persistent limitations, including cellular immaturity, incomplete vascularization and systemic integration, model variability, and limited clinical validation. We further discuss how integration of bioengineering, genome editing, multi-omics, and computational methods may improve predictive performance. Standardization, interlaboratory validation, regulatory qualification, and prospective benchmarking against human clinical outcomes will be essential for translating these platforms into reliable tools for cardiovascular research and therapeutic development. Collectively, the convergence of stem cell biology, bioengineering, genome editing, multi-omics, and computational approaches is establishing a new generation of human-centered cardiovascular models with the potential to strengthen mechanistic discovery and accelerate the development of more predictive and personalized therapies.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664009/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Podocyte Metabolic Flexibility Under Stress Conditions: From Metabolic Adaptation to Maladaptive Responses.","authors":"Marine Thirion, Emmanuel Esteve, Vanessa Tagliatti, Anne-Emilie Declèves","doi":"10.3390/cells15191751","DOIUrl":"10.3390/cells15191751","url":null,"abstract":"<p><p>Podocytes are essential for glomerular function by maintaining the integrity of the glomerular filtration barrier. As terminally differentiated, post-mitotic cells, they are highly vulnerable to injury, which represents a central event in the development of chronic kidney disease. Although podocytes have been extensively studied to elucidate their structure and function, their metabolism and the role of metabolic dysregulation in podocyte injury remain incompletely understood. This review summarizes current knowledge of podocyte metabolism and its responses to diverse stressors. We discuss the basal metabolic profile of podocytes, which remains a matter of debate in the literature, with a focus on mitochondrial function. We further examine how stress conditions such as gluco- and lipotoxicity, vasoactive stress, mechanical stress, and immune dysregulation induce metabolic adaptations that become maladaptive upon sustained exposure. Metabolic reprogramming and its consequences, including cytoskeletal disorganization, are reviewed alongside emerging therapeutic strategies aimed at restoring podocyte metabolic homeostasis. A better understanding of podocyte metabolic flexibility may provide innovative strategies to preserve podocyte integrity and prevent the progression of chronic kidney disease.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"15 19","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13664509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149191723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}