摘要
铁死亡作为近年新发现的依赖于铁和活性氧的调节细胞死亡形式,与心肌缺血再灌注损伤(MIRI)的发生密切相关,其可通过铁代谢、氨基酸代谢、脂质代谢以及内质网应激、自噬相关通路等途径导致MIRI。心肌梗死后MIRI与心脏功能的持续性损害有关,可造成心肌细胞的致命性损伤。铁死亡是MIRI致病过程中的一种细胞死亡,对其进行靶向治疗有助于心肌细胞的实质性保护。因此,深入研究铁死亡与MIRI之间的关系可以为MIRI的治疗提供新思路。
Ferroptosis,as a newly discovered form of cell death that relies on iron and reactive oxygen species,is closely related to the occurrence of myocardial ischemia-reperfusion injury(MIRI).It can cause MIRI through pathways such as iron metabolism,amino acid metabolism,lipid metabolism,endoplasmic reticulum stress,and autophagy related pathways.MIRI is associated with sustained damage to cardiac function after myocardial infarction,which can cause fatal damage to myocardial cells.Ferroptosis is a type of cell death in the pathogenesis of MIRI,and targeted treatment can help to provide substantial protection for myocardial cells.Therefore,in-depth research on the relationship between ferroptosis and MIRI can provide new ideas for the treatment of MIRI.
作者
马西元
唐强
尹侠
李宇婷
孟享泓
李宏玉
MA Xiyuan;TANG Qiang;YIN Xia;LI Yuting;MENG Xianghong;LI Hongyu(Heilongjiang University of Chinese Medicine,Harbin 150040,China;Department of Rehabilitation Medicine,the Second Affiliated Hospital of Heilongjiang University of Chinese Medicine,Harbin 150001,China)
出处
《医学综述》
CAS
2023年第20期4034-4038,共5页
Medical Recapitulate
基金
黑龙江省博士后资助项目(LBH-Z20201)
黑龙江中医药大学研究生创新科研项目(2022yjscx007)。
关键词
心肌缺血再灌注损伤
铁死亡
心肌细胞
Myocardial ischemia-reperfusion injury
Ferroptosis
Cardiomyocytes
