JOURNAL OF CELLULAR AND MOLECULAR MEDICINE最新文献

{"title":"Cartilage Extracellular Matrix Homeostasis in Knee Osteoarthritis: Pathomechanisms and Therapeutic Targeting","authors":"Chao Du,&nbsp;Jiwei Zhong,&nbsp;Jialin Yang,&nbsp;Yanbo Huang,&nbsp;Qi Liu,&nbsp;Dongdong Cao,&nbsp;Tianci Guo,&nbsp;Jida Wang,&nbsp;Aifeng Liu","doi":"10.1111/jcmm.71384","DOIUrl":"10.1111/jcmm.71384","url":null,"abstract":"<p>Knee osteoarthritis (KOA) is a degenerative joint disease primarily driven by the disruption of homeostasis in the chondrocyte extracellular matrix (CECM). This review systematically examines the central role of CECM homeostasis in KOA pathogenesis and summarizes recent advances in this field. We synthesized contemporary basic and clinical research to analyse the mechanisms underlying CECM homeostatic imbalance. These include biomechanical stress, inflammatory responses, programmed cell death (e.g., apoptosis, pyroptosis, ferroptosis), impaired autophagy, and cellular senescence. We also evaluated intrinsic risk factors and the application of related biomarkers for diagnosis and prognosis. Our analysis identifies multifaceted pathways driving CECM imbalance and highlights promising multi-modal therapeutic strategies. These include novel pharmacological agents (e.g., high-purity chondroitin sulphate, natural active monomers), physical and regenerative therapies (e.g., stem cells, platelet-rich plasma), precision interventions (e.g., gene editing, RNA interference), and tissue engineering approaches (e.g., smart biomaterials, biomimetic scaffolds). The evidence demonstrates that these strategies can effectively modulate CECM metabolism, promote cartilage repair, and slow disease progression. Targeting CECM homeostasis is a core strategy for developing disease-modifying therapies for KOA. Future efforts should focus on interdisciplinary integration, individualized precision medicine, and multi-site synergistic interventions. This review provides a comprehensive foundation for innovating strategies to delay or reverse KOA progression by restoring CECM balance.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149170169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RIPC Protects Against Renal Ischaemia–Reperfusion Injury by Activating SIRT3/Parkin-Mediated Mitophagy","authors":"Qian Cui,&nbsp;Lina Zhao,&nbsp;Wenjun Dai,&nbsp;Shuyan Sun,&nbsp;Yinan Li,&nbsp;Chenghui Zhou,&nbsp;Hanjun Pei","doi":"10.1111/jcmm.71372","DOIUrl":"10.1111/jcmm.71372","url":null,"abstract":"<p>Remote ischaemic preconditioning (RIPC) protects against renal ischaemia–reperfusion injury (IRI), yet its precise mechanism remains incompletely understood, particularly regarding the role of mitochondrial quality control. This study investigated whether SIRT3-dependent mitophagy mediates the protective effects of RIPC against acute kidney injury (AKI) induced by IRI and further examined the integrity of mitophagic flux and involvement of the classic Parkin-mediated mitophagic pathway. We used a murine bilateral renal ischaemia–reperfusion injury (IRI) model, including RIPC pretreatment, 3-methyladenine (3-MA) intervention and SIRT3 knockout intervention, and a HK-2 cell hypoxia/reoxygenation (H/R) model, including SIRT3 siRNA knockdown, SIRT3 overexpression and chloroquine (CQ) intervention. Renal function, histopathological changes, apoptosis, mitochondrial membrane potential and mitophagy were assessed using biochemical analysis, histological and TUNEL staining, JC-1 staining, transmission electron microscopy, mitochondrial protein analysis and immunofluorescence colocalization of Parkin and LC3B. RIPC improved renal function, alleviated tubular injury and apoptosis, and enhanced mitophagy in mice, which was attenuated by SIRT3 knockout or 3-MA. In HK-2 cells, RIPC plasma protected against H/R injury and activated mitophagic flux, as verified by CQ treatment, while SIRT3 knockdown abolished these effects and SIRT3 overexpression maintained protective mitophagy levels. RIPC pretreatment restored the IRI-induced reduction in Parkin and LC3B colocalization in renal tubular epithelial mitochondria, and this effect was attenuated by 3-MA. RIPC alone had no detectable cytotoxicity or effect on basal mitophagy. In conclusion, RIPC mitigates renal IRI by activating SIRT3-dependent mitophagy, with involvement of the Parkin-mediated mitophagic pathway. Our in vivo and in vitro data support the central role of SIRT3 in RIPC-induced renoprotection and provide evidence for an intact mitophagic flux mechanism.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655216/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149164913","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haematopoietic Cells Deficient for Calreticulin or Expressing Its Oncogenic Variants Maintain Functional Antigen Presentation","authors":"Maria Höhrhan,&nbsp;Laura Antonio-Herrera,&nbsp;Henrique G. Colaço,&nbsp;Anja Wagner,&nbsp;Markus Unterwurzacher,&nbsp;Cecilia Varga,&nbsp;Klaus Kratochwill,&nbsp;Andreas Bergthaler,&nbsp;Robert Kralovics","doi":"10.1111/jcmm.71399","DOIUrl":"10.1111/jcmm.71399","url":null,"abstract":"<p>Intact antigen presentation in cancer cells is a key prerequisite for endogenous anticancer T cell responses and a starting point for immunotherapy. Calreticulin was postulated as a chaperone and integral part of the peptide-loading complex of MHC-I. Oncogenic mutations of calreticulin allow surface expression in complex with the thrombopoietin receptor, leading to ligand-independent activation, cell proliferation, and myeloproliferative neoplasms. We hypothesized that mutated calreticulin could also corrupt the function of MHC-I, as previous reports revealed decreased surface expression, peptide-loading defects and retention of MHC-I in the Golgi apparatus. We employed reporter cell models that utilized the T cell response towards target murine and human primary cells and cell lines carrying calreticulin mutations as a functional readout. We also harnessed T cell responses upon a viral infection In Vivo. We found no evidence for immunosuppression in mutant calreticulin-expressing or calreticulin-deficient cells. Our study implies an overestimation of the significance of calreticulin for MHC-I functionality and provides an impulse for reevaluation. Furthermore, we show that calreticulin deficiency affects only a few proteins, including myeloperoxidase and other proteins involved in antibacterial immune mechanisms. In conclusion, mutant calreticulins do not interfere with antigen presentation in MPN, making MHC-I-dependent immunotherapies a viable venue for treatment.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655222/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149169173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single-Cell Multiomics Reveals That OTUD7B Is a Central Driver of Epithelial Remodelling and the Immunosuppressive Microenvironment in Pancreatic Ductal Adenocarcinoma","authors":"Xiao-Li Liu,&nbsp; Jing-Wang,&nbsp;Shan-Yu Zhao,&nbsp; Lu-Li,&nbsp;Ming-Hui Zhang","doi":"10.1111/jcmm.71322","DOIUrl":"10.1111/jcmm.71322","url":null,"abstract":"<p>Pancreatic ductal adenocarcinoma (PAAD) is characterized by extreme malignancy and profound resistance to therapy, largely driven by a fibrotic and immunosuppressive tumour microenvironment (TME). The deubiquitinase OTU domain-containing protein 7B (OTUD7B) has been implicated in inflammatory and oncogenic signalling, but its role in PAAD and its TME remains unclear. This study integrated single-cell RNA-seq datasets from the GEO and bulk RNA-seq data from the TCGA to delineate the cellular ecosystem of PAAD, and employed cell–cell communication analysis, high-dimensional weighted gene coexpression network analysis (hdWGCNA), and nonnegative matrix factorization (NMF) to identify OTUD7B-associated modules and epithelial subpopulations, while assessing the survival and clinicopathologic correlations of OTUD7B in the TCGA-PAAD cohort. Quantitative proteomics of OTUD7B-knockout PAAD cells was performed and combined with GO/KEGG and GSEA to explore downstream pathways, and immune infiltration was inferred by deconvolution algorithms and validated by multiplex immunofluorescence staining of OTUD7B, CD4, and FOXP3. Single-cell RNA-seq revealed the expansion of epithelial cells, fibroblasts, and macrophages with dense ligand–receptor networks, alongside the depletion of effector T and NK cells, indicating a shift toward an immunosuppressive TME. hdWGCNA identified epithelial–ECM modules in which OTUD7B served as a hub gene, and NMF revealed an OTUD7B-high epithelial subset enriched in glycosylation-related metabolic programs and positioned at an early stage of the malignant trajectory. OTUD7B was significantly upregulated in PAAD and was associated with higher grade, lymph node metastasis, and advanced stage, and predicted poorer overall survival. Proteomic profiling of OTUD7B-deficient cells revealed broad remodelling of mitochondrial oxidative phosphorylation, ROS metabolism, and redox homeostasis. OTUD7B expression was positively correlated with M2 macrophage infiltration, immunomodulatory gene expression, and CD4⁺FOXP3⁺ regulatory T-cell accumulation, and tissue staining further confirmed the positive association between OTUD7B expression and Treg-rich regions. Collectively, OTUD7B acts as a key integrative node that links epithelial remodelling, mitochondrial metabolic reprogramming, and TME immunosuppression in PAAD, serving as an adverse prognostic biomarker and a potential therapeutic target to remodel tumour metabolism and enhance antitumor immunity.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13655224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149166477","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Unfolded Protein Response as a Modulator of Cancer-Immune Cell Communication in the Tumour Microenvironment","authors":"Yew Hwang Chee,&nbsp;Matthieu Moncan,&nbsp;Eileen Reidy,&nbsp;Adrienne M. Gorman,&nbsp;Afshin Samali","doi":"10.1111/jcmm.71380","DOIUrl":"10.1111/jcmm.71380","url":null,"abstract":"<p>The tumour microenvironment (TME) comprises a dynamic network of structural, cellular, and signalling components that interact to influence tumour development. Immune cells play a key role in recognizing and eliminating cancer cells through detection of tumour-derived membrane and secreted proteins processed in the endoplasmic reticulum (ER). These ER-matured proteins on target cells act as critical communication signals, coordinating immune responses against tumour cells. However, during tumorigenesis, accumulation of unfolded or misfolded proteins in the ER of the cancer cells triggers the unfolded protein response (UPR), a transcriptional program that alleviates proteotoxic stress by reshaping the cancer cell proteome and secretome, thereby promoting survival. Activation of UPR disrupts intercellular communication and ultimately impairs immune-mediated tumour clearance. Understanding this crosstalk could inform the development of therapeutics targeting UPR-driven immune modulation. This review discusses how UPR-signalling modulates tumour-immune cell interactions within the TME.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/jcmm.71380","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149136839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Kappa-Opioid Receptor/Dynorphin System in Modulating Neural-Circuits of Depression and Anxiety—A Review","authors":"Cristian Ciotei,&nbsp;Horia Păunescu,&nbsp;Cristina Lungu,&nbsp;Adriana-Alexandra Marica,&nbsp;Mihai Florin Tănase,&nbsp;Ruxandra-Cristina Marin,&nbsp;Mihnea Costescu,&nbsp;Ion Fulga,&nbsp;Oana Andreia Coman","doi":"10.1111/jcmm.71392","DOIUrl":"10.1111/jcmm.71392","url":null,"abstract":"<p>Major depression and anxiety disorders are psychiatric disorders that involve a great number of people. There is a growing need for new and better pharmacological treatments for these diseases. Kappa-opioid receptor (KOR) antagonists seem to be a promising new pathway for the development of new antidepressants and anxiolytics, but a great challenge is understanding how the various neural circuits work and to what degree they are influenced by KOR modulators. This narrative review is focussed on two main circuits: the Hippocampus-Amygdala-Prefrontal Cortex and the Ventral Tegmental Area-Nucleus Accumbens. The relevant neuroanatomy, their role in modulating behaviour and how KOR modulators can alleviate these diseases are discussed. Concluding, a more holistic understanding of the circuits influenced by the KOR/Dyn system is relevant for developing new therapies. In non-clinical pharmacology addressed to the KOR/Dyn system, variables such as age, sex and social hierarchy rank can influence experimental outcomes.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13643048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘‘YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR–HIF1α–LHDA Axis”","authors":"","doi":"10.1111/jcmm.71370","DOIUrl":"10.1111/jcmm.71370","url":null,"abstract":"<p>\u0000 <span>Z. Liu</span>, <span>T. Jiang</span>, <span>P. Li</span>, et al., “ <span>YTHDF3 Mediates the Occurrence and Development of Breast Cancer by Regulating Glycolysis Through the mTOR-HIF1α-LHDA Axis</span>,” <i>Journal of Cellular and Molecular Medicine</i> <span>30</span>, no. <span>9</span>(<span>2024</span>), e18271, https://doi.org/10.1111/jcmm.71105.\u0000 </p><p>In Ziqian Liu et al., the representative experimental images for MCF-7 cells shown in Figures 2C, F and G contain image misuse resulting from careless manual handling and technical error made during figure assembly. The correct figure is shown below. The authors confirm all results and conclusions of this article remain unchanged.</p><p>We apologize for this error.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639706/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Serum Leptin Exacerbates Osteoarthritis by Promoting Subchondral Bone H-Type Vessel Angiogenesis via Activation of the PI3K/AKT Pathway’","authors":"","doi":"10.1111/jcmm.71376","DOIUrl":"10.1111/jcmm.71376","url":null,"abstract":"<p>\u0000 <span>R. Li</span>, <span>Z. Xi</span>, <span>S. Luo</span>, <span>J. Qin</span>, <span>T. Liu</span>, and <span>J. Zhang</span>, “ <span>Serum Leptin Exacerbates Osteoarthritis by Promoting Subchondral Bone H-Type Vessel Angiogenesis via Activation of the PI3K/AKT Pathway</span>,” <i>Journal of Cellular and Molecular Medicine</i> <span>30</span>, no. <span>13</span> (<span>2026</span>): e71232, https://doi.org/10.1111/jcmm.71232\u0000 </p><p>In Figure 6A(c), the representative CD31/EMCN immunofluorescence image for the DMM BKS+ZSTK474 group was inadvertently duplicated from the DMM ob/ob group during figure assembly. The correct representative CD31/EMCN immunofluorescence image for the DMM BKS+ZSTK474 group is shown below.</p><p>We apologize for this error.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639715/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipid Accumulation Promotes Tumorigenic Behaviour of Colorectal Cancer Cells","authors":"Tatjana Itzenhäuser,&nbsp;Fulya Suzan Schildt,&nbsp;Seraphine Jochem,&nbsp;Judith Sommer,&nbsp;Michael Stürzl,&nbsp;Elisabeth Naschberger,&nbsp;Anja Katrin Boßerhoff,&nbsp;Claus Hellerbrand","doi":"10.1111/jcmm.71393","DOIUrl":"10.1111/jcmm.71393","url":null,"abstract":"<p>Obesity and hyperlipidemia are risk factors for the development and progression of different types of cancer including colorectal cancer (CRC). The underlying mechanisms are only incompletely understood. The aim of this study was to assess the impact of hyperlipidemic conditions on tumorigenic behaviour of CRC cells and the effect of obesity on lipid metabolism in CRC tissues. Oleic acid complexed to albumin was added to the cell culture medium of human colon cancer cell lines HT29, Caco-2, HCT116, LoVo, SW480 and SW48. This led to a time- and dose-dependent uptake of oleate and triglyceride accumulation and increased expression of perilipin-2 (PLIN2), a structural component of lipid droplets and carnitine palmitoyltransferase 1 A (CPT1A), the key enzyme of beta-oxidation. Furthermore, proliferation, migratory activity and the expression of epithelial-mesenchymal transition (EMT) markers and the proinflammatory cytokine interleukin-8 (IL-8) were dose-dependently increased in CRC cells. In tumorous tissues of obese CRC patients, PLIN2 expression tended to be higher than in tissues of CRC patients with normal weight and immunohistological analysis showed a stronger PLIN2 immunosignal and Ki67-staining a higher proliferative index in CRC tissues of obese patients. Furthermore, we observed a significant correlation between PLIN2 and CPT1A expression in human CRC tissues and CRC patients with high PLIN2 or CPT1A expression showed a poorer overall and disease-free survival. In conclusion, our data indicate that fatty acid uptake promotes tumorigenicity of CRC cells. The exogenous uptake of fatty acids could be particularly important in obesity associated hyperlipidemia and herewith may be a critical factor by which obesity promotes CRC progression. Here, these findings support further evaluation of the structural protein PLIN2 as tumour marker as well as therapeutic target in CRC patients.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13634124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110139","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to ‘Sirtuin 3 Is Essential for Hypertension-Induced Cardiac Fibrosis via Mediating Pericyte Transition’","authors":"","doi":"10.1111/jcmm.71388","DOIUrl":"10.1111/jcmm.71388","url":null,"abstract":"<p>\u0000 <span>Su, H</span>, <span>Zeng, H</span>, <span>Liu, B</span>, <span>Chen, J-X</span>. <span>Sirtuin 3 Is Essential for Hypertension-Induced Cardiac Fibrosis via Mediating Pericyte Transition</span>. <i>Journal of Cellular and Molecular Medicine</i> <span>2020</span>; <span>24</span>: <span>8057</span>–<span>8068</span>. https://doi.org/10.1111/jcmm.15437\u0000 </p><p>In Figure 6A of the DHE-stained image for the control WT group, the image was incorrect. The correct image is shown below.</p><p>In Figure 5A, the same GAPDH band as in Figure 2D was used, as TGF-β1 and β-MHC were from the same PVDF membrane and shared the same GAPDH band.</p><p>Figure 5A and 5B (NG2-DsRed mice). (A) Low-magnification (20X) overview showing the regional expression profile of TGF-β1 (green); the co-stained cell marker channel is omitted here for visual clarity of overall expression levels. (B) High-magnification (40X) individual channels and merged view of the identical tissue section, demonstrating co-localization of TGF-β1 (green) with NG2-DsRed (red) to identify the cell source. The bounding box indicates the region magnified in Panel B.</p><p>We apologize for this error.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"30 19","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13633526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149110201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}