NLRP3炎症小体与心肌缺血再灌注损伤的研究进展

Progress of NLRP3 Inflammasome and Myocardial Ischemia Reperfusion Injury

及时再通阻塞的冠状动脉是降低急性心肌梗死患者死亡率的关键,但实现再灌注的同时可能对缺血的心肌造成二次损伤,即心肌缺血再灌注损伤(myocardial ischemia reperfusion injury,MIRI)。核苷酸结合寡聚化结构域样受体蛋白3(nucleotide binding oligomerization domain⁃like receptor protein 3,NLRP3)炎症小体通过促进心肌细胞焦亡、级联放大炎症反应和破坏心肌血管内皮细胞,参与了MIRI的整个过程,引起了临床广泛关注。目前,以NLRP3炎症小体及其调节因子为药物靶点的相关研究正在如火如荼地开展,有望为MIRI的预防和治疗提供新的思路。

Timely recanalization of blocked coronary arteries is the key to reduce the mortality of acute myocardial infarction,but reperfusion may cause secondary injury to ischemic myocardium,namely myocardial ischemia reperfusion injury(MIRI).Nucleotide binding oligomerization domain⁃like receptor protein 3(NLRP3)inflammasome is involved in the whole process of MIRI by promoting cardiomyocyte scortosis,proin⁃flammatory effects of cascade amplification and destruction of myocardial vascular endothelial cells,which has attracted extensive clinical attention.At the same time,related studies on NLRP3 inflammasome and its regula⁃tory factors as drug targets are in full flow,which is expected to provide new ideas for the prevention and treat⁃ment of MIRI.