心肌缺血再灌注损伤中铁死亡的调控机制研究进展  

Regulatory Mechanisms of Ferroptosis in Myocardial Ischemia Reperfusion Injury

作　　者：叶宇恒 钱玲玲[1] 王如兴[1] 李库林[1] YE Yuheng;QIAN Lingling;WANG Ruxing;LI Kulin(Department of Cardiology,Wuxi People’s Hospital Affiliated to Nanjing Medical University,Wuxi 214023,Jiangsu,China)

机构地区：[1]南京医科大学附属无锡医院无锡市人民医院心内科,江苏无锡214023

出　　处：《心血管病学进展》2023年第5期416-419,共4页Advances in Cardiovascular Diseases

基　　金：国家自然科学基金面上项目(81770331)。

摘　　要：心肌缺血再灌注损伤是一种涉及多种细胞病理生理过程及细胞信号通路的现象,常发生于冠心病和心搏骤停复苏等心血管不良事件后。铁死亡是一种由铁参与的细胞脂质过氧化物积累,抗脂质过氧化物活性减退导致的程序性细胞死亡方式。近年研究表明,铁死亡与心肌缺血再灌注损伤密切相关,氧化还原失衡、脂质过氧化和内质网应激等多种细胞事件参与了铁死亡的调控。现主要概述心肌缺血再灌注损伤中铁死亡的机制及相关治疗新思路。Myocardial ischemia reperfusion injury is a phenomenon involving varieties of cellular pathophysiological processes and cellular signaling pathways,which often occurs after cardiovascular adverse events like coronary heart disease and resusciation of cardiac arrest.Ferroptosis is a programmed cell death mode caused by the accumulation of cellular lipid peroxides and the decrease in activity of anti lipid peroxides,which is involved in iron.Recent studies show that ferroptosis is closely related to myocardial ischemia reperfusion injury.Cell events,such as redox imbalance,lipid peroxidation and endoplasmic reticulum stress,participate in the regulation of ferroptosis.This article reviews the mechanisms of ferroptosis in myocardial ischemia reperfusion injury and related new horizons for cardiac treatment.

关 键 词：心肌缺血再灌注损伤 铁死亡 谷胱甘肽过氧化物酶4 

分 类 号：R54[医药卫生—心血管疾病]