Association of Circulating Autophagy Proteins ATG5 and Beclin 1 with Acute Myocardial Infarction in a Case-Control Study.

IF 1.9 4区 医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS Cardiology Pub Date : 2024-01-01 Epub Date: 2024-03-02 DOI:10.1159/000537816
Marie-Hélène Grazide, Jean-Bernard Ruidavets, Wim Martinet, Meyer Elbaz, Cécile Vindis
{"title":"Association of Circulating Autophagy Proteins ATG5 and Beclin 1 with Acute Myocardial Infarction in a Case-Control Study.","authors":"Marie-Hélène Grazide, Jean-Bernard Ruidavets, Wim Martinet, Meyer Elbaz, Cécile Vindis","doi":"10.1159/000537816","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>Acute myocardial infarction (AMI) is a main contributor of sudden cardiac death worldwide. The discovery of new biomarkers that can improve AMI risk prediction meets a major clinical need for the identification of high-risk patients and the tailoring of medical treatment. Previously, we reported that autophagy a highly conserved catabolic mechanism for intracellular degradation of cellular components is involved in atherosclerotic plaque phenotype and cardiac pathological remodeling. The crucial role of autophagy in the normal and diseased heart has been well described, and its activation functions as a pro-survival process in response to myocardial ischemia. However, autophagy is dysregulated in ischemia/reperfusion injury, thus promoting necrotic or apoptotic cardiac cell death. Very few studies have focused on the plasma levels of autophagy markers in cardiovascular disease patients, even though they could be companion biomarkers of AMI injury. The aims of the present study were to evaluate (1) whether variations in plasma levels of two key autophagy regulators autophagy-related gene 5 (ATG5) and Beclin 1 (the mammalian yeast ortholog Atg6/Vps30) are associated with AMI and (2) their potential for predicting AMI risk.</p><p><strong>Methods: </strong>The case-control study population included AMI patients (n = 100) and control subjects (n = 99) at high cardiovascular risk but without known coronary disease. Plasma levels of ATG5 and Beclin 1 were measured in the whole population study by enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Multivariate analyses adjusted on common cardiovascular factors and medical treatments, and receiver operating characteristic curves demonstrated that ATG5 and Beclin 1 levels were inversely associated with AMI and provided original biomarkers for AMI risk prediction.</p><p><strong>Conclusion: </strong>Plasma levels of autophagy regulators ATG5 and Beclin 1 represent relevant candidate biomarkers associated with AMI.</p>","PeriodicalId":9391,"journal":{"name":"Cardiology","volume":null,"pages":null},"PeriodicalIF":1.9000,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11152019/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cardiology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000537816","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/3/2 0:00:00","PubModel":"Epub","JCR":"Q3","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0

Abstract

Introduction: Acute myocardial infarction (AMI) is a main contributor of sudden cardiac death worldwide. The discovery of new biomarkers that can improve AMI risk prediction meets a major clinical need for the identification of high-risk patients and the tailoring of medical treatment. Previously, we reported that autophagy a highly conserved catabolic mechanism for intracellular degradation of cellular components is involved in atherosclerotic plaque phenotype and cardiac pathological remodeling. The crucial role of autophagy in the normal and diseased heart has been well described, and its activation functions as a pro-survival process in response to myocardial ischemia. However, autophagy is dysregulated in ischemia/reperfusion injury, thus promoting necrotic or apoptotic cardiac cell death. Very few studies have focused on the plasma levels of autophagy markers in cardiovascular disease patients, even though they could be companion biomarkers of AMI injury. The aims of the present study were to evaluate (1) whether variations in plasma levels of two key autophagy regulators autophagy-related gene 5 (ATG5) and Beclin 1 (the mammalian yeast ortholog Atg6/Vps30) are associated with AMI and (2) their potential for predicting AMI risk.

Methods: The case-control study population included AMI patients (n = 100) and control subjects (n = 99) at high cardiovascular risk but without known coronary disease. Plasma levels of ATG5 and Beclin 1 were measured in the whole population study by enzyme-linked immunosorbent assay.

Results: Multivariate analyses adjusted on common cardiovascular factors and medical treatments, and receiver operating characteristic curves demonstrated that ATG5 and Beclin 1 levels were inversely associated with AMI and provided original biomarkers for AMI risk prediction.

Conclusion: Plasma levels of autophagy regulators ATG5 and Beclin 1 represent relevant candidate biomarkers associated with AMI.

查看原文
分享 分享
微信好友 朋友圈 QQ好友 复制链接
本刊更多论文
一项病例对照研究显示,循环中的自噬蛋白 ATG5 和 Beclin 1 与急性心肌梗死有关。
导言:急性心肌梗死(AMI)是全球心脏性猝死的主要诱因。发现能改善急性心肌梗死风险预测的新生物标志物,满足了识别高危患者和调整治疗方案的重大临床需求。此前,我们曾报道自噬是细胞内降解细胞成分的一种高度保守的代谢机制,它参与了动脉粥样硬化斑块表型和心脏病理重塑。自噬在正常和患病心脏中的关键作用已经得到了充分的描述,它的激活在心肌缺血时起到了促进存活的作用。然而,自噬在缺血/再灌注损伤时会失调,从而促进心脏细胞坏死或凋亡。很少有研究关注心血管疾病患者血浆中的自噬标记物水平,尽管它们可能是急性心肌梗死损伤的辅助生物标记物。本研究的目的是评估1)两种关键自噬调节因子 ATG5(自噬相关基因 5)和 Beclin 1(哺乳动物酵母的直向同源物 Atg6/Vps30)的血浆水平变化是否与急性心肌梗死有关;2)它们预测急性心肌梗死风险的潜力:病例对照研究人群包括AMI患者(100人)和心血管高危但无已知冠心病的对照组(99人)。通过酶联免疫吸附法测定整个研究人群血浆中ATG5和Beclin 1的水平:根据常见心血管因素和治疗方法进行调整的多变量分析以及接收器操作特征曲线(ROC)表明ATG5和Beclin 1水平与急性心肌梗死成反比,为预测急性心肌梗死风险提供了新的生物标志物:结论:血浆中自噬调节因子 ATG5 和 Beclin 1 的水平代表了与急性心肌梗死相关的候选生物标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 去求助
来源期刊
Cardiology
Cardiology 医学-心血管系统
CiteScore
3.40
自引率
5.30%
发文量
56
审稿时长
1.5 months
期刊介绍: ''Cardiology'' features first reports on original clinical, preclinical and fundamental research as well as ''Novel Insights from Clinical Experience'' and topical comprehensive reviews in selected areas of cardiovascular disease. ''Editorial Comments'' provide a critical but positive evaluation of a recent article. Papers not only describe but offer critical appraisals of new developments in non-invasive and invasive diagnostic methods and in pharmacologic, nutritional and mechanical/surgical therapies. Readers are thus kept informed of current strategies in the prevention, recognition and treatment of heart disease. Special sections in a variety of subspecialty areas reinforce the journal''s value as a complete record of recent progress for all cardiologists, internists, cardiac surgeons, clinical physiologists, pharmacologists and professionals in other areas of medicine interested in current activity in cardiovascular diseases.
期刊最新文献
Gender Differences in Cardiovascular Disease: Perspectives on Disparities in Women's Treatment and Outcomes. Meta-analysis of the efficacy and safety of radiofrequency catheter ablation for pediatric paroxysmal supraventricular tachycardia. Floppy Mitral Valve/Mitral Valve Prolapse and Manifestations Not Related to Mitral Regurgitation: Time to Search the Dark Side of the Moon. Impact of an exercise-based cardiac rehabilitation program on cardiopulmonary test parameters. Prevalence and predictors of thromboembolic events in patients with left ventricular dysfunction and left ventricular thrombus.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
已复制链接
已复制链接
快去分享给好友吧!
我知道了
×
扫码分享
扫码分享
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1