Article(id=1291404475898524510, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404401374130524, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.05.024, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1726761600000, receivedDateStr=2024-09-20, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824420188, onlineDateStr=2026-08-04, pubDate=1742140800000, pubDateStr=2025-03-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824420188, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824420188, creator=13701087609, updateTime=1785824420188, updator=13701087609, issue=Issue{id=1291404401374130524, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='5', pageStart='601', pageEnd='750', issueExtLink='null', onlineDate='null', pubDate='1742140800000', pubDateStr='2025-03-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824402421, creator='13701087609', updateTime=1785897165150, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1291709590438170760, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404401374130524, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1291709590438170761, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404401374130524, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=722, endPage=726, ext={EN=ArticleExt(id=1291404477668520799, articleId=1291404475898524510, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research status of STAT3-mediated signaling network regulation of airway remodeling in asthma, columnId=1246531408630534361, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Airway remodeling is one of the pathological features of asthma and the direct cause of irreversible decline in lung function in asthma patients. Signal transducer and activator of transcription 3 (STAT3) can drive the differentiation of helper tlymphocyt (Th)2 and Th17 cells and the expression of cytokines. It plays a key regulatory role in airway remodeling processes such as metaplasia of bronchial epithelial goblet cells (GC), deposition of extracellular matrix (ECM), and epithelial mesenchymal transition (EMT) induced by proliferation of airway smooth muscle cells (ASMCs) in asthma. Therefore, the regulation of asthma airway remodeling related signal networks by STAT3 has become a new research hotspot in recent years. This article reviews the mechanism of STAT3 in regulating asthma airway remodeling from the perspective of signaling networks such as Janus kinase 2 (JAK2), nuclear factor kappa B (NF-κB), transforming growth factor-β1 (TGF-β1), interleukin-17 (IL-17), IL-6, providing a theoretical basis for the study of asthma airway remodeling mechanisms and the development of new drugs.

, authors=Yue ZHANG, Zhi-wang WANG, Ke-ting HUANG, Ke-ke LIANG, Yue ZHAO, Ping QUAN, authorsList=Yue ZHANG, Zhi-wang WANG, Ke-ting HUANG, Ke-ke LIANG, Yue ZHAO, Ping QUAN, authorCompany=null, correspAuthors=Zhi-wang 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=1291404477928567648, articleId=1291404475898524510, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=STAT3介导的信号网络调控哮喘气道重塑的研究现状, columnId=1246531408819278046, journalTitle=中国临床药理学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

气道重塑是哮喘主要病理特征之一，也是哮喘患者肺功能不可逆性降低的直接原因。信号转导与转录激活因子3（STAT3）可驱动辅助型T细胞（Th）2、Th17细胞分化及其细胞因子的表达，在哮喘气道上皮杯状细胞（GC）化生、细胞外基质（ECM）沉积以及气道平滑肌细胞（ASMCs）增殖引起的上皮-间质转化（EMT）等气道重塑过程中发挥了关键的调控作用，故STAT3调控哮喘气道重塑相关信号网络已成为近年来研究的新热点。本文从Janus激酶2（JAK2）、核因子-κB（NF-κB）、转化生长因子-β1（TGF-β1）、白细胞介素-17（IL-17）以及IL-6等信号网络的角度，综述STAT3调控哮喘气道重塑的作用机制，为哮喘气道重塑机制研究以及新药研发提供理论依据。

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张悦（2001-），女，硕士研究生，主要从事呼吸系统疾病药物的相关研究

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张悦（2001-），女，硕士研究生，主要从事呼吸系统疾病药物的相关研究

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