Article(id=1317885786930918367, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, articleNumber=null, orderNo=null, doi=10.12449/JCH260835, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1767542400000, receivedDateStr=2026-01-05, revisedDate=null, revisedDateStr=null, acceptedDate=1772985600000, acceptedDateStr=2026-03-09, onlineDate=1792138056738, onlineDateStr=2026-10-16, pubDate=1787587200000, pubDateStr=2026-08-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792138056738, onlineIssueDateStr=2026-10-16, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792138056738, creator=13701087609, updateTime=1792138056738, updator=13701087609, issue=Issue{id=1317885672153797495, tenantId=1146029695717560320, journalId=1316781422847033486, year='2026', volume='42', issue='8', pageStart='1745', pageEnd='2000', issueExtLink='null', onlineDate='null', pubDate='1787587200000', pubDateStr='2026-08-25', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=1, specialIssue=null, createTime=1792138029373, creator='13701087609', updateTime=1792138608261, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317888100290900262, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317888100290900263, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1980, endPage=1984, ext={EN=ArticleExt(id=1317885787161605088, articleId=1317885786930918367, tenantId=1146029695717560320, journalId=1316781422847033486, language=EN, title=Mechanism of action of T cell senescence in the progression of liver fibrosis to liver cirrhosis in elderly patients with chronic hepatitis B, columnId=1317885737828205560, journalTitle=Journal of Clinical Hepatology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Liver fibrosis is a key pathological process in the transition from chronic liver disease to cirrhosis，especially in elderly patients with chronic hepatitis B，and this process is characterized by rapid progression and poor prognosis. T cell function gradually declines with aging，and T cell senescence is recognized as a key immunological mechanism accelerating the progression of liver fibrosis. Current studies have shown that senescent T cells promote the transition from liver fibrosis to liver cirrhosis by altering the liver inflammatory microenvironment，modulating the activity of fibrosis-related cells，and impairing immune surveillance function. This article systematically reviews the molecular mechanisms of T cell senescence and its role in the progression of liver fibrosis in elderly patients with chronic hepatitis B，as well as novel therapeutic approaches targeting immunosenescence with reference to the latest immunological findings and stem cell-based therapeutic strategies，so as to provide theoretical support for precise intervention for such patients.

, authors=Ting Wang, Chengkai Yang, Xu Xu, authorsList=Ting Wang, Chengkai Yang, Xu Xu, authorCompany=null, correspAuthors=Xu Xu, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1317885790835815395, articleId=1317885786930918367, tenantId=1146029695717560320, journalId=1316781422847033486, language=CN, title=T细胞衰老在老年慢性乙型肝炎患者肝纤维化向肝硬化进展中的作用机制, columnId=1317885739623367674, journalTitle=临床肝胆病杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

肝纤维化是慢性肝病向肝硬化转变的关键病理过程，尤其在老年慢性乙型肝炎患者中，该过程进展迅速且预后较差。随着年龄增长，T细胞功能逐渐衰退，T细胞衰老被认为是加速肝纤维化进展的重要免疫学机制。当前研究表明，衰老T细胞通过改变肝脏炎症微环境、调节纤维化相关细胞活性及削弱免疫监视功能，促进肝纤维化向肝硬化的转化。本文系统综述了T细胞衰老的分子机制及其在老年慢性乙型肝炎肝纤维化进展中的作用，结合最新免疫学发现及干细胞治疗策略，探讨靶向免疫衰老的新型治疗途径，旨在为此类患者的精准干预提供理论支持。

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DOI: 10.2196/17904., articleTitle=Regenerative therapy for liver cirrhosis based on intrahepatic arterial infusion of autologous subcutaneous adipose tissue-derived regenerative (stem) cells: Protocol for a confirmatory multicenter uncontrolled clinical trial, refAbstract=null)], funds=null, companyList=[AuthorCompany(id=1317885791079085028, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885786930918367, xref=null, ext=[AuthorCompanyExt(id=1317885791083279333, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885786930918367, companyId=1317885791079085028, language=EN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=Department of General Practice，Ganmei Hospital Affiliated to Kunming Medical University，Kunming 650224，China), AuthorCompanyExt(id=1317885791091667942, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885786930918367, companyId=1317885791079085028, language=CN, country=null, province=null, city=null, postcode=null, companyName=null, departmentName=null, remark=昆明医科大学附属甘美医院全科医学科，昆明 650224)])], figs=[ArticleFig(id=1317885794413556736, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885786930918367, language=EN, label=Figure 1, caption=Mechanisms of senescent T cells in liver fibrosis/cirrhosis, figureFileSmall=RlXitbszScK3/vMnaOn0UQ==, figureFileBig=MSUUM0ton7oN4dhhV+egeA==, tableContent=null), ArticleFig(id=1317885794497441792, tenantId=1146029695717560320, journalId=1316781422847033486, articleId=1317885786930918367, language=CN, label=图1, caption=衰老T细胞在肝纤维化/肝硬化中的机制

注：HBV，乙型肝炎病毒；HCV，丙型肝炎病毒；CD28^-、CD57⁺，衰老T细胞标志物表现为共刺激分子CD28的丧失及细胞毒性相关CD57表达增加；PD-1，程序性死亡受体1，在衰老T细胞中表达增加；SASP，衰老相关分泌表型；IL-6，白细胞介素6；IL-17，白细胞介素17；TGF-β，转化生长因子β；TNF-α，肿瘤坏死因子α；HSC，肝星状细胞；ECM，细胞外基质。

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