焦亡在心肌缺血再灌注损伤中的作用及相关治疗药物研究进展

The Role of Pyroptosis in Myocardial Ischemia-reperfusion Injury and the Research Progress of Related Therapeutic Drugs

细胞焦亡是近几年来通过研究发现的由半胱天冬氨酸特异性蛋白酶介导Gasdermin D蛋白发挥作用,引发的新的程序性促炎类型细胞坏死,在形态和病理生理上均不同于其它形式的细胞死亡(如凋亡、坏死)。最新研究表明,细胞焦亡参与心肌缺血再灌注损伤(MIRI)。MIRI是急性心肌梗死(AMI)患者经积极血运重建后仍有较高死亡率发生的首要原因之一。部分基于细胞焦亡相关信号通路的药物,在保护心血管疾病模型中发挥了特定作用。本文主要对细胞焦亡在MIRI中的病理生理机制及相关治疗药物影响细胞焦亡并应用于MIRI防治方面进行综述。

In recent years,it has been discovered that pyroptosis is a new programmed pro-inflammatory type of cell necrosis triggered by cysteinyl-specific proteinase(Caspase)mediating the action of Gasdermin D(GSDMD)protein.It differs from other forms of cell death(such as apoptosis and necrosis)in morphologically and pathophysiologically.Recent studies have shown that pyroptosis is involved in myocardial ischemia-reperfusion injury(MIRI),which is one of the main reasons for leading causes of high mortality in patients with myocardial infarction despite aggressive hemodialysis.Some drugs based on the pyroptosis related signaling pathway,exerted specific effects in protecting cardiovascular disease models.This article mainly reviews the pathophysiological mechanisms of pyroptosis in MIRI and the effect of related therapeutic drugs on pyroptosis and its application in the prevention and treatment of MIRI.