Article(id=1211269164648493662, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1211269157790806494, articleNumber=null, orderNo=null, doi=10.11855/j.issn.0577-7402.2021.04.12, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=research-article, receivedDate=1604332800000, receivedDateStr=2020-11-03, revisedDate=1609171200000, revisedDateStr=2020-12-29, acceptedDate=null, acceptedDateStr=null, onlineDate=1766718673144, onlineDateStr=2025-12-26, pubDate=1619539200000, pubDateStr=2021-04-28, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1766718673144, onlineIssueDateStr=2025-12-26, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1766718673144, creator=13701087609, updateTime=1766718673144, updator=13701087609, issue=Issue{id=1211269157790806494, tenantId=1146029695717560320, journalId=1189873630562394117, year='2021', volume='46', issue='4', pageStart='319', pageEnd='424', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=0, createTime=1766718671510, creator=13701087609, updateTime=1766718756000, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1211269512217882745, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1211269157790806494, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1211269512217882746, tenantId=1146029695717560320, journalId=1189873630562394117, issueId=1211269157790806494, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=393, endPage=397, ext={EN=ArticleExt(id=1211269165030175348, articleId=1211269164648493662, tenantId=1146029695717560320, journalId=1189873630562394117, language=EN, title=Research progress on the relation of ATF6 to cardiovascular diseases, columnId=1190243275882729994, journalTitle=Medical Journal of Chinese People’s Liberation Army, columnName=Review, runingTitle=null, highlight=null, articleAbstract=

Activated transcription factor 6 (ATF6) is a transmembrane glycoprotein located in the endoplasmic reticulum.It exists widely in various tissues including myocardium and participates in endoplasmic reticulum stress (ERS) by regulating the unfolded protein response (UPR) signal pathway, which has become one of the major regulators of organs/tissues homeostasis and is of great significance in signal transduction, gene expression and protein synthesis. A number of studies have shown that ATF6 plays an important regulatory role in the occurrence and development of atherosclerosis, myocardial infarction, cardiac hypertrophy, diabetic cardiomyopathy, arrhythmia and other common cardiovascular diseases (CVD). At present, some studies have proved that ATF6 can regulate its activity and function to intervene the occurrence and development of some CVD. As a result, whether a small molecule regulator can be designed to treat some CVD by regulating ATF6 has become a research hot-spot. ATF6-based therapies have made great progress and have shown promising efficacy in small animal models of CVD and other systemic protein-based diseases. The small molecule regulator to ATF6 has a broad application prospect in cardiovascular disease, but further basic and clinical studies are still needed to lay the theoretical and practical foundation for its application. In present paper, the structure, classification and correlation of ATF6 with CVD are reviewed in order to provide references for experimental researches, clinical diagnoses and treatments of CVD.

, correspAuthors=Zheng Zhang, 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=Pei Wang, Yu Peng, Zheng Zhang), CN=ArticleExt(id=1211269165516714640, articleId=1211269164648493662, tenantId=1146029695717560320, journalId=1189873630562394117, language=CN, title=激活转录因子6与心血管疾病关系的研究进展, columnId=1190243276029530637, journalTitle=解放军医学杂志, columnName=综述, runingTitle=null, highlight=null, articleAbstract=

激活转录因子6(ATF6)是一种位于内质网的跨膜糖蛋白，广泛分布于包括心肌在内的多种组织，主要通过调节未折叠蛋白反应信号通路来参与内质网应激，是器官及组织稳态的主要调节因子之一。多项研究表明，ATF6在动脉粥样硬化、心肌梗死、心肌肥厚、糖尿病心肌病及心律失常等常见心血管疾病的发生发展中均起着重要的调控作用。该文就ATF6的结构、分型及其与心血管疾病的关系进行综述，以期为心血管疾病的实验研究及临床诊疗提供参考。

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王沛，硕士研究生，主要从事心血管疾病方面的研究

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王沛，硕士研究生，主要从事心血管疾病方面的研究

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