Article(id=1317885785823629867, tenantId=1146029695717560320, journalId=1316781422847033486, issueId=1317885672153797495, articleNumber=null, orderNo=null, doi=10.12449/JCH260836, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1763654400000, receivedDateStr=2025-11-21, revisedDate=null, revisedDateStr=null, acceptedDate=1768924800000, acceptedDateStr=2026-01-21, onlineDate=1792138056474, onlineDateStr=2026-10-16, pubDate=1787587200000, pubDateStr=2026-08-25, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1792138056474, onlineIssueDateStr=2026-10-16, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1792138056474, creator=13701087609, updateTime=1792138056474, 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=1985, endPage=1989, ext={EN=ArticleExt(id=1317885786071093804, articleId=1317885785823629867, tenantId=1146029695717560320, journalId=1316781422847033486, language=EN, title=Role and mechanism of liver sinusoidal endothelial cells in acetaminophen-induced liver injury, columnId=1317885737828205560, journalTitle=Journal of Clinical Hepatology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Liver injury due to acetaminophen overdose is one of the main causes of acute liver failure，with a complex pathogenesis. In this process，liver sinusoidal endothelial cell （LSEC） injury is a key early event jointly mediated by factors such as oxidative stress，cell apoptosis，and imbalance between fibrinolysis and coagulation. Subsequent LSEC dysfunction further induces sinusoidal microcirculatory disturbances，amplifies the inflammatory response，impairs the regeneration and repair abilities of the liver，and finally causes hepatocyte necrosis. This article systematically elaborates on the critical role and molecular mechanism of LSEC in acetaminophen-induced liver injury，in order to provide a theoretical basis for novel therapeutic strategies and research directions.

, authors=Lu Peng¹, Qi Zhang², Xinxin Zhu³, Aijuan Qu², Yan Wang¹, authorsList=Lu Peng, Qi Zhang, Xinxin Zhu, Aijuan Qu, Yan Wang, authorCompany=null, correspAuthors=Yan Wang, 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=1317885788847723055, articleId=1317885785823629867, tenantId=1146029695717560320, journalId=1316781422847033486, language=CN, title=肝窦内皮细胞在对乙酰氨基酚所致肝损伤中的作用及其机制, columnId=1317885739623367674, journalTitle=临床肝胆病杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

对乙酰氨基酚过量所致肝损伤是急性肝衰竭的主要病因之一，其机制复杂。在此过程中，肝窦内皮细胞损伤是关键的早期环节，由氧化应激、细胞凋亡、纤溶/凝血系统失衡等因素共同介导。由此引发的肝窦内皮细胞功能障碍，会进一步造成肝窦微循环紊乱、炎症反应放大，并损害肝脏的再生修复能力，最终导致肝细胞坏死。本文旨在系统阐述肝窦内皮细胞在对乙酰氨基酚诱导肝损伤中的关键作用及其分子机制，以期为开发新的治疗策略与研究方向提供理论依据。

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注：APAP，对乙酰氨基酚；NAPQI，N-乙酰基-P-苯醌亚胺；GSH，谷胱甘肽；TLR9，Toll样受体9；NLRP3，核苷酸结合寡聚结构域样受体家族热蛋白结构域相关蛋白3；saa1/2，血清淀粉样物质A1/2；TLR2，Toll样受体2；VCAM-1，血管细胞黏附分子1；PAR1，蛋白酶激活受体1；PAR4，蛋白酶激活受体4；ATP，腺苷三磷酸；LSEC，肝窦内皮细胞；VE-cadherin，钙黏蛋白；H₂O₂，过氧化氢，GTPase，鸟苷三磷酸酶；G12/13，鸟嘌呤核苷酸结合蛋白α12/13亚基；Gαq，鸟嘌呤核苷酸结合蛋白αq亚基。

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