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.Howev...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.展开更多
基金the National Natural Science Foundation of China(81670259 to M.X.and 82000247 to S.-a.S.).
文摘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.