Cell Regeneration最新文献

{"title":"Systemic regeneration medicines for muscular dystrophy: progress and challenges in pro-regenerative drug development.","authors":"So-Ichiro Fukada, Atsushi Kubo, Motoi Kanagawa, Yoshitsugu Aoki","doi":"10.1186/s13619-026-00296-8","DOIUrl":"10.1186/s13619-026-00296-8","url":null,"abstract":"<p><p>Regenerative medicine has the potential to restore lost organ and tissue functions, and research on cell transplantation is steadily advancing toward clinical application. However, significant challenges remain in developing cell therapies for skeletal muscle, largely because the human body contains more than 600 individual muscles, making it impractical to treat all affected muscles through local transplantation alone. One strategy to overcome this limitation is to enhance the intrinsic regenerative capacity of muscle through various modalities; in this review, we define these approaches as pro-regenerative drugs. Histone deacetylase (HDAC) inhibitors provide a compelling example, demonstrating that stimulation of endogenous muscle regeneration can confer therapeutic benefits in the genetic disease Duchenne muscular dystrophy (DMD). This raises a fundamental question: why do pro-regenerative drugs provide durable benefits without Dystrophin restoration? This review summarizes the current status and importance of pro-regenerative drug development and discusses why sustained therapeutic effects can be achieved despite the lack of gene complementation. It also highlights key pathways that promote muscle regeneration as potential targets for future therapies.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13333570/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390026","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":"Generation of human chemically induced pluripotent stem cells from UC-MSCs.","authors":"Guangqiang Gong, Shanshan Wen, Siyi Huang, Ran Liu, Ran Zheng, Wei Jiang","doi":"10.1186/s13619-026-00295-9","DOIUrl":"10.1186/s13619-026-00295-9","url":null,"abstract":"","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13319313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148359817","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":"Standard: human breast cancer organoids derived from diverse clinical sample sources.","authors":"Zhigang Chen, Ningning Xu, Ming Chen, Jianming Hu, Zhuohang Yu, Sangsang Zhu, Yi Zhang, Ronghao Zhang, Kun Wang, Shu Wang, Dong Gao, Fei Ma, Jin Zhang, Jiong Wu, Binghe Xu, Erwei Song, Jian Huang","doi":"10.1186/s13619-026-00291-z","DOIUrl":"10.1186/s13619-026-00291-z","url":null,"abstract":"<p><p>Breast cancer remains a leading cause of cancer-related morbidity and mortality worldwide, driven by therapeutic resistance, recurrence, and metastasis. Patient-derived organoids (PDOs) have emerged as a robust platform that preserves histopathological, genetic, and functional features of parental tumors, enabling translational research and precision oncology. However, the lack of standardized procedures across laboratories limits reproducibility and clinical applicability. Here, we present a consensus-oriented standard for the establishment, characterization, quality control and application of human breast cancer organoids derived from diverse clinical sources, including surgical tissues, biopsies, pleural effusion, ascites, and circulating tumor cells (CTCs). This document defines key terminologies, outlines standardized workflows, and introduces quantitative validation criteria for successful organoid establishment. In addition, it provides structured guidance for advanced models, including immune-tumor, neuro-tumor, and microbiota-tumor organoid systems, with defined functional validation endpoints. Standardized protocols for drug sensitivity testing are also proposed, including seeding density, exposure duration, and response metrics such as IC50 and AUC. Representative validation strategies, including histological, molecular and functional concordance with parental tumors, are incorporated to enhance reproducibility and translational relevance. This standard aims to harmonize methodologies, improve cross-study comparability, and accelerate the clinical implementation of breast cancer organoid-based precision medicine.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13269618/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148257392","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":"Olfactory epithelium regeneration and homeostasis: cellular and molecular mechanisms and novel methodological advances.","authors":"Jiaming Qi, Yiqun Yu","doi":"10.1186/s13619-026-00292-y","DOIUrl":"10.1186/s13619-026-00292-y","url":null,"abstract":"<p><p>The olfactory epithelium (OE) maintains lifelong neurogenesis and shows strong regenerative capacity through the coordinated functions of horizontal basal cells (HBCs) and globose basal cells (GBCs). These progenitors are regulated by key transcriptional factors such as Sox2, p63, Pax6, Ascl1, Neurog1 and NeuroD1, as well as signaling pathways including Wnt/β-catenin, Notch, YAP and inflammation-related regulators, which together control lineage specification and injury-induced plasticity. A set of genes such as Lgr5, Tmem59, Notch1, and Chil4 play critical roles in OE homeostasis and regeneration, depending on a broader and highly dynamic network. Recent progress in single-cell transcriptomics, spatial transcriptomics and organoid models has revealed previously unrecognized cell states, differentiation routes and intercellular communications. This review summarizes the molecular and cellular mechanisms that support OE regeneration and highlights emerging technologies that advance understanding the process of olfactory epithelium regeneration and guiding future approaches for restoring olfactory function.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13230444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148143005","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":"Tollip antagonizes ESCRT-III-mediated plasma membrane repair and cell recovery.","authors":"Julia M Ferrick, Xinan Meng, Emily Morgan, Anthony Kalvi, Zhen Li, Chaoqun Li, Chao-Yuan Chang, Suhong Xu, Yi-Nan Gong","doi":"10.1186/s13619-026-00289-7","DOIUrl":"10.1186/s13619-026-00289-7","url":null,"abstract":"<p><p>Cells can recover from sub-lethal necrosis by repairing plasma-membrane (PM) rupture through the ESCRT-III machinery, but how this process is regulated remains unknown. Here, we identify Toll-interacting protein (Tollip) as a conserved negative regulator for ESCRT-III-mediated PM repair. Quantitative proteomics revealed the enrichment of Tollip at damaged PM. Additionally, microscopy assays in mammalian cells and C. elegans confirmed the recruitment of Tollip to PM injury sites. Tollip deficiency augmented ESCRT-III assembly, improved long-term cell survival after sub-lethal PM damage, and enhanced PM repair, whereas Tollip overexpression suppressed these processes. Tollip translocation occurred independently of Ca²⁺ influx, different from ESCRT-III. Functionally, by limiting PM repair and maintaining sub-lethal PM integrity loss, Tollip ensured optimal chemokine and cytokine production from the plasma-membrane-integrity (PMI) pathway, which is directly triggered by PM ruptures. Thus, Tollip acts as a molecular rheostat that links membrane damage repair and cell recovery to immune signaling.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13187079/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147970702","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":"Advances in the application of human amniotic membrane for tissue repair.","authors":"Jiatong Han, Xinyue Yang, Arooj Khabbir, Chun Hu, Yidan Gao, Xinran Liu, Renping Liu, Yuyang Zhang, Yang Lei","doi":"10.1186/s13619-026-00290-0","DOIUrl":"10.1186/s13619-026-00290-0","url":null,"abstract":"<p><p>Human amniotic membrane (hAM) is a widely used biomaterial with longstanding utility in ophthalmology and emerging therapeutic promise across orthopaedics, obstetrics and gynaecology, and dermatology. Clinically available biological tissue repair materials primarily encompass autologous, allogeneic, and xenogeneic tissues. However, autologous materials are limited by availability, while allogeneic and xenogeneic tissues often present challenges related to immunocompatibility. As a commonly used allogeneic biomaterial, the hAM is regarded as a highly promising tissue repair material owing to its favourable immunological profile and exceptional tissue-regenerative properties. HAM is the innermost natural barrier of the placenta and possesses unique structural and biological characteristics that facilitate tissue repair and regeneration. This review summarizes recent advances and clinical applications of hAM in orthopaedics, obstetrics and gynaecology, and dermatology, specifically focusing on its roles in promoting tendon repair, alleviating osteoarthritis, repairing endometrial injury, treating diabetic foot ulcer, and enhancing burn wound healing. With the continued development of regenerative medicine, hAM is expected to play an increasingly important role in diverse tissue repair and regenerative medicine applications.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13156383/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147855993","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":"Cellular senescence in skeletal muscle regeneration.","authors":"Xingyuan Liu, Huating Wang","doi":"10.1186/s13619-026-00287-9","DOIUrl":"10.1186/s13619-026-00287-9","url":null,"abstract":"<p><p>Skeletal muscle possesses a remarkable capacity for regeneration, driven by the activation and proliferation of Pax7-positive muscle stem cells within a dynamic niche that includes immune cells, fibro-adipogenic progenitors, endothelial cells, pericytes, and neural elements. Cellular senescence, a stress-induced program featuring stable cell-cycle arrest and the senescence-associated secretory phenotype (SASP), has emerged as a critical yet paradoxical regulator of this process. Accumulating evidence indicates that transient senescence, particularly in FAPs, macrophages, and other niche cells during acute muscle injury, plays a beneficial role in supporting muscle regeneration. These senescent cells promote cellular plasticity, enhance myoblast differentiation, facilitate phagocytic clearance of debris, and modulate inflammation and repair via timely SASP factor secretion. However, conflicting findings suggest that senescent cells exert detrimental effects, impairing regeneration by establishing a sustained pro-inflammatory and pro-fibrotic niche, especially when senescence persists in aged or dystrophic muscle. This review synthesizes the complex and contradictory roles of cellular senescence in skeletal muscle regeneration, underscores the distinction between transient pro-regenerative and persistent deleterious senescence, highlights the importance of cell-type-specific contributions, and emphasizes the need for precise characterization of senescent cell dynamics and fate. Resolving these discrepancies will be critical for developing targeted senotherapeutic strategies to enhance muscle regeneration in aging and degenerative diseases.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147833817","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":"MSI1-FTHL17C-iron circuit couples metabolic and epigenetic control of pluripotency in mouse embryonic stem cells.","authors":"Qianyan Li, Yi Li, Jiazhen Han, Liming Cheng, Gufa Lin, Youwei Chen","doi":"10.1186/s13619-026-00288-8","DOIUrl":"10.1186/s13619-026-00288-8","url":null,"abstract":"<p><p>Maintenance of pluripotency in embryonic stem cells (ESCs) requires coordinated integration of transcriptional, metabolic, and epigenetic programs. Here, we identify a post-transcriptional regulatory axis linking the RNA-binding protein Musashi-1 (MSI1) to iron dependent DNA demethylation via the ferritin like gene Fthl17c. Genetic ablation of MSI1 and its short isoform MSI1-C in mESCs induced spontaneous differentiation and was accompanied by downregulation of Fthl17 family genes. Among these, Fthl17c was directly bound and stabilized by MSI1, and its depletion reduced intracellular ferrous iron (Fe²⁺), impaired ten eleven translocation (TET) enzyme activity, and increased global 5-methylcytosine (5mC) levels. Restoration of Fthl17c expression rescued TET activity, reduced DNA methylation, and reinstated pluripotency associated gene expression, whereas extracellular Fe²⁺ supplementation alone was insufficient. In contrast, vitamin C, which preserves redox active Fe²⁺, effectively restored DNA demethylation, highlighting the requirement for bioavailable iron in TET mediated epigenetic regulation. Biochemical and imaging analyses further revealed that FTHL17C interacts with TET1 in the nucleus, supporting a role in facilitating iron dependent catalysis. Together, these findings define an MSI1-FTHL17C-Fe²⁺-TET axis that integrates post transcriptional control of iron homeostasis with epigenetic remodeling to preserve the pluripotent and plastic state of embryonic stem cells.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149808/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834100","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":"Recent advances in TGF-β signaling: insights into regulation, pathophysiological function, and clinical translation.","authors":"Xiaohua Yan, Junyu Zhang, Carl-Henrik Heldin, Xin-Hua Feng, Ye-Guang Chen","doi":"10.1186/s13619-026-00286-w","DOIUrl":"10.1186/s13619-026-00286-w","url":null,"abstract":"<p><p>Cytokines from the transforming growth factor-β (TGF-β) superfamily are essential regulators of cell growth, survival, and differentiation, playing a pivotal role in mammalian embryonic development, adult tissue homeostasis, and progression of human diseases. Recently, an international symposium on TGF-β Signaling in Development and Diseases was held in Nanchang, China, from October 21 to 23, 2025. This event showcased the latest advances in TGF-β signaling and its pathophysiological functions. Over ten presentations at the symposium offered new insights on Smad-dependent and non-Smad TGF-β signaling, its spatiotemporal regulation, and multifaceted roles of TGF-β family cytokines in various pathophysiological contexts. The symposium also addressed potential strategies and opportunities for targeting the TGF-β pathway in the treatment of human diseases.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13121644/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763843","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":"HUMSCs repair CCl₄-induced chronic liver injury in rats via metabolic regulation.","authors":"Changpeng Xie, Yiming Dong, Xinxin Yin, Jin Zeng, Zhanhai Su, Haiyan Wang, Jing Zhao, Qiong Wu, Panjian Wei, Ziyu Wang, Meng Gu, Xudong Zhang, Xianzong Ma, Yong Deng, Yuanming Pan, Juan An","doi":"10.1186/s13619-026-00282-0","DOIUrl":"10.1186/s13619-026-00282-0","url":null,"abstract":"<p><strong>Background and aims: </strong>To explore the therapeutic effects of human umbilical cord mesenchymal stem cells (HUMSCs) on repairing CCl₄-induced chronic liver injury in rats via intravenous injection and to identify the associated key metabolites.</p><p><strong>Methods: </strong>Cell experiments: THLE-2 cells were divided into blank control, CCl₄-treated, and CCl₄ + Exos groups. Cell viability was assessed using the CCK-8 assay, while levels of AST, ALT, and MDA were determined using commercial kits. Targeted metabolomics analysis was employed to identify differentially expressed metabolites. Transmission electron microscopy (TEM) was used to evaluate mitochondrial morphology, and immunofluorescence staining was performed to examine the colocalization of Exos with mitochondria. Animal experiments: 24 healthy SPF SD rats were randomly divided into healthy, CCl₄, and CCl₄ + HUMSCs groups (n = 8 per group). Serum samples were collected for biochemical detection and targeted metabolomics analyses, while liver tissues underwent histopathological examination. Immunofluorescence staining was employed to monitor HUMSCs enrichment.</p><p><strong>Results: </strong>In the CCl₄ + Exos group, cell viability was significantly restored, and the elevated levels of AST, ALT, and MDA were reversed, while mitochondrial ultrastructure was ameliorated with successful Exos-mitochondria colocalization. Targeted metabolomics confirmed the presence of differentially expressed metabolites exhibiting consistent trends in both cellular and animal models. In the animal study, the CCl₄ group showed significant liver dysfunction and hepatic pathology characterized by hepatocyte steatosis and fibrous tissue hyperplasia. In contrast, the CCl₄ + HUMSCs group demonstrated markedly improved liver function and reduced pathological changes. Biochemical analysis revealed significant differences in ALT, AST, ALB, TBIL, TP, UREA, CR, and UA levels between the CCl₄ + HUMSCs and CCl₄ groups. Serum metabolomics analysis showed that compared with the CCl₄ group, 1,7-Dimethylxanthine and Xanthosine were significantly upregulated, while Succinic Acid, (S)-2-Hydroxybutanoic Acid, oxidized glutathione, and 3'-Sialyllactose were significantly downregulated in the CCl₄ + HUMSCs group.</p><p><strong>Conclusion: </strong>HUMSCs treatment significantly reduced hepatic steatosis and fibrosis compared with the CCl₄ group alone. Metabolomic analysis suggests that the underlying mechanisms may involve upregulation of propanoate metabolism and increased taurochenodeoxycholic acid levels, which warrant further investigation.</p>","PeriodicalId":9811,"journal":{"name":"Cell Regeneration","volume":"15 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12996463/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147472648","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}