Article(id=1203033502368363151, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2023.05.0609, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1645459200000, receivedDateStr=2022-02-22, revisedDate=null, revisedDateStr=null, acceptedDate=1655308800000, acceptedDateStr=2022-06-16, onlineDate=1764755138245, onlineDateStr=2025-12-03, pubDate=1685203200000, pubDateStr=2023-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1764755138245, onlineIssueDateStr=2025-12-03, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1764755138244, creator=13701087609, updateTime=1764755138244, updator=13701087609, issue=Issue{id=1203033494428541350, tenantId=1146029695717560320, journalId=1189873630562394117, year='2023', volume='48', issue='5', pageStart='489', pageEnd='626', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1764755136353, creator=13701087609, updateTime=1764756085669, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1203037476202967229, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1203037476202967230, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1203033494428541350, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=609, endPage=614, ext={EN=ArticleExt(id=1203033503588905646, articleId=1203033502368363151, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress of mesenchymal stem cells and their modifiers in treatment of liver fibrosis, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Liver fibrosis is a response to chronic liver injury caused by a variety of factors, such as alcohol consumption, viral hepatitis, autoimmune hepatitis, non-alcoholic steatohepatitis (NASH), non-alcoholic fatty liver disease (NAFLD) and cholestatic liver disease. The combined effect of all these factors on the liver is to produce chronic inflammation leading to an abnormal wound-healing response. Mesenchymal stem cells (MSCs) are pluripotent stem cells that are able to implant into target tissues and secrete a variety of factors that can alter or improve the function of damaged tissues. Stem cells have the advantages of self-renewal, pluripotent differentiation and low immunogenicity. Due to their differentiation potential and paracrine characteristics, MSCs are the key for repair. This review focuses on the mechanism and progress of MSCs and their modifiers in liver fibrosis.

, correspAuthors=Lin Wang, authorNote=null, correspAuthorsNote=, 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, authorCompany=null, fund=null, authors=null, authorsList=Jian Ding, Liang Song, Bai Ruan, Lin Wang), CN=ArticleExt(id=1203033504209662695, articleId=1203033502368363151, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=间充质干细胞及其修饰体在肝纤维化治疗中的作用研究进展, columnId=1190243276029530637, journalTitle=解放军医学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

肝纤维化是由饮酒、病毒性肝炎、自身免疫性肝炎、非酒精性脂肪性肝炎（NASH）、非酒精性脂肪性肝病（NAFLD）及胆汁淤积肝脏疾病等多种因素引起的慢性肝损伤，上述因素对肝脏的共同影响是产生慢性炎症，导致异常的肝脏炎症、坏死、再生、修复过程。间充质干细胞（MSCs）是一种多能干细胞，能够植入靶组织并分泌多种因子，从而改变或改善受损组织的功能。干细胞具有自我更新、多潜能分化及低免疫原性等优点，因此MSCs的分化潜力及旁分泌特性使其成为组织修复的重要选择。本文主要就MSCs及其修饰体在肝纤维化治疗中的作用及研究进展进行综述。

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MSCs. 间充质干细胞；HSCs. 肝星状细胞；IC. 炎性因子

, figureFileSmall=PevfK/6eeJ//oKyLC8F+Gg==, figureFileBig=0Kw1Cbi5WA+0ct51aSVBjQ==, tableContent=null), ArticleFig(id=1203033507829347253, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1203033502368363151, language=EN, label=Tab. 1, caption=

Mechanisms of different MSCs modifications in treatment of liver fibrosis

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修饰体类型	修饰体结构	作用机制
药物协同修饰	(1)辛伐他汀联合BMSCs (Sim-MSCs) (2)IFN-γ预处理BMSCs(γ-SEVs)的细胞外小泡 (3)褪黑素(MT)修饰MSCs	(1)降低硫代乙酰胺诱导的肝硬化大鼠肝胶原分布，通过抑制TGF-β/Smad信号转导发挥强大的抗肝纤维化保护作用 (2)在肝硬化肝中可以抗炎巨噬细胞及调节性T细胞的诱导多种作用 (3)改善细胞归巢以及更好地维持基质降解与积累之间的平衡
细胞因子修饰	(1)HGF修饰人脐静脉MSCs (2)人MMP1修饰BMSCs (3)过表达HNF-4α修饰MSCs	(1)减轻Ⅰ型及Ⅲ型胶原的沉积，降低CCl4诱导的大鼠肝纤维化中α-SMA、TGF-β1、Smad2及Smad3的表达 (2)MMP1基因可能增强BMSCs的抗纤维化作用 (3)增强NF-κB依赖性抗炎作用
miRNA修饰	(1)miR-181-5p修饰脂肪MSCs (2)miR-145-5p修饰人脐血MSCs外泌体	(1)通过抑制STAT3/Bcl-2/Beclin 1信号通路增加自噬，从而减轻TGF-β1诱导的肝纤维化 (2)通过下调FSCN1表达减轻CCl4诱导的肝纤维化

), ArticleFig(id=1203033507925816254, tenantId=1146029695717560320, journalId=1189873630562394117, articleId=1203033502368363151, language=CN, label=表1, caption=

不同MSCs修饰体治疗肝纤维化的机制

, figureFileSmall=null, figureFileBig=null, tableContent=

修饰体类型	修饰体结构	作用机制
药物协同修饰	(1)辛伐他汀联合BMSCs (Sim-MSCs) (2)IFN-γ预处理BMSCs(γ-SEVs)的细胞外小泡 (3)褪黑素(MT)修饰MSCs	(1)降低硫代乙酰胺诱导的肝硬化大鼠肝胶原分布，通过抑制TGF-β/Smad信号转导发挥强大的抗肝纤维化保护作用 (2)在肝硬化肝中可以抗炎巨噬细胞及调节性T细胞的诱导多种作用 (3)改善细胞归巢以及更好地维持基质降解与积累之间的平衡
细胞因子修饰	(1)HGF修饰人脐静脉MSCs (2)人MMP1修饰BMSCs (3)过表达HNF-4α修饰MSCs	(1)减轻Ⅰ型及Ⅲ型胶原的沉积，降低CCl4诱导的大鼠肝纤维化中α-SMA、TGF-β1、Smad2及Smad3的表达 (2)MMP1基因可能增强BMSCs的抗纤维化作用 (3)增强NF-κB依赖性抗炎作用
miRNA修饰	(1)miR-181-5p修饰脂肪MSCs (2)miR-145-5p修饰人脐血MSCs外泌体	(1)通过抑制STAT3/Bcl-2/Beclin 1信号通路增加自噬，从而减轻TGF-β1诱导的肝纤维化 (2)通过下调FSCN1表达减轻CCl4诱导的肝纤维化

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