Cardiac Piezo1 Exacerbates Lethal Ventricular Arrhythmogenesis by Linking Mechanical Stress with Ca^(2+) Handling After Myocardial Infarction  

作　　者：Sheng-an Su Yuhao Zhang Wudi Li Yutao Xi Yunrui Lu Jian Shen Yuankun Ma Yaping Wang Yimin Shen Lan Xie Hong Ma Yao Xie Meixiang Xiang 

机构地区：[1]Department of Cardiology,Cardiovascular Key Laboratory of Zhejiang Province,The Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310009,China [2]Department of Endocrinology,The Second Affiliated Hospital,Zhejiang University School of Medicine,Hangzhou 310009,China [3]Texas Heart Institute,Houston,TX 77030,USA

出　　处：《Research》2024年第1期583-594,共12页研究（英文）

基　　金：the National Natural Science Foundation of China(81670259 to M.X.and 82000247 to S.-a.S.).

摘　　要：Ventricular arrhythmogenesis is a key cause of sudden cardiac death following myocardial infarction(MI).Accumulating data show that ischemia,sympathetic activation,and inflammation contribute to arrhythmogenesis.However,the role and mechanisms of abnormal mechanical stress in ventricular arrhythmia following MI remain undefined.We aimed to examine the impact of increased mechanical stress and identify the role of the key sensor Piezo1 in ventricular arrhythmogenesis in MI.Concomitant with increased ventricular pressure,Piezo1,as a newly recognized mechano-sensitive cation channel,was the most up-regulated mechanosensor in the myocardium of patients with advanced heart failure.Piezo1 was mainly located at the intercalated discs and T-tubules of cardiomyocytes,which are responsible for intracellular calcium homeostasis and intercellular communication.

关 键 词：VENTRICULAR HOMEOSTASIS VENTRICULAR 

分 类 号：R542.22[医药卫生—心血管疾病]