Article(id=1292135535942857185, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.10.010, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1774886400000, receivedDateStr=2026-03-31, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785998718485, onlineDateStr=2026-08-06, pubDate=1779897600000, pubDateStr=2026-05-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785998718485, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785998718485, creator=13701087609, updateTime=1785998718485, updator=13701087609, issue=Issue{id=1292135425250976333, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='10', pageStart='1351', pageEnd='1500', issueExtLink='null', onlineDate='null', pubDate='1779897600000', pubDateStr='2026-05-28', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785998692095, creator='13701087609', updateTime=1786014373634, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292201198489202995, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292201198489202996, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292135425250976333, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=1409, endPage=1416, ext={EN=ArticleExt(id=1292135536165155298, articleId=1292135535942857185, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Mechanisms of tyrosine kinase inhibitors-induced cardiotoxicity: A research update, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Tyrosine kinase inhibitors (TKIs) are targeted anticancer drugs that block signaling pathways like EGFR, VEGFR, and BCR-ABL. While they have greatly improved cancer patient survival, frequently cause cardiotoxic effects such as left ventricular dysfunction and life-threatening arrhythmias—problems that pose a growing challenge in clinical practice. The mechanisms behind this toxicity include on-target damage, off-target effects, and electrical disturbances in the heart. Newly discovered mechanisms—such as metabolic reprogramming, non-coding RNA regulation, and the gut microbiota-heart axis—have also been linked to TKIs-induced cardiotoxicity. This article aims to systematically review the mechanism of TKIs-induced cardiotoxicity, provide directions for future exploration of the emerging mechanisms of TKIs-induced cardiotoxicity, and provide a theoretical basis for the development of new intervention drugs.

, authors=Kang-jia ZUO^1a, Xiao-li ZHANG^1a, Yong-ming MEI^1a, Yao ZHANG^1a, Xiao-chun WANG^1b, authorsList=Kang-jia ZUO, Xiao-li ZHANG, Yong-ming MEI, Yao ZHANG, Xiao-chun WANG, authorCompany=null, correspAuthors=Xiao-chun 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=1292135538178421219, articleId=1292135535942857185, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=酪氨酸激酶抑制剂致心脏毒性机制的研究进展, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

酪氨酸激酶抑制剂（TKIs）是一类肿瘤治疗靶向药物，其通过特异性阻断EGFR、VEGFR、BCR-ABL等信号通路发挥抗肿瘤作用。该类药物的临床应用显著改善了肿瘤患者的生存期，然而，TKIs在抗肿瘤时常诱发左室功能障碍、恶性心律失常等心脏毒性，这些心脏毒性已成为临床治疗过程中的重要挑战。TKIs致心脏毒性的机制涉及靶点依赖性损伤、非靶点损伤效应及电生理紊乱等。近年来，一些新兴机制被发现与TKIs导致的心脏毒性有关，包括代谢重编程、非编码RNA调控、肠道菌群-心脏轴等。本文旨在系统回顾TKIs致心脏毒性的作用机制，为未来探究TKIs致心脏毒性的新兴机制提供方向，新型干预药物的研发提供理论基础。

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左康家（1991-），男，实验师，主要从事抗肿瘤药物心血管毒性研究

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左康家（1991-），男，实验师，主要从事抗肿瘤药物心血管毒性研究

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