NLRP3炎症小体在心肌缺血再灌注损伤中的研究进展

Research Progress of NLRP3 Inflammasome in Myocardial Ischemia-Reperfusion Injury

心肌缺血再灌注损伤(MIRI)制约着心肌梗死后血运重建的临床疗效,甚至可造成急性心力衰竭、心肌抑顿、致命性心律失常等,因此探索MIRI的发病机制是目前心血管疾病的研究热点。炎症反应始终贯穿MIRI的病理过程,核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体作为机体防御反应的重要调控因子,可以通过激活下游炎症因子驱动并放大炎症反应,介导细胞和组织的损伤,是MIRI疾病发展中的重要环节。选择性调控NLRP3炎症小体可以为临床MIRI的保护治疗提供新靶标。

Myocardial ischemia-reperfusion injury(MIRI)restricts the clinical efficacy of revascularization after myocardial infarction,and may even cause acute heart failure,myocardial stunning,fatal arrhythmia and so on.Therefore exploration of the pathogenesis of MIRI is a hot topic in the research of cardiovascular diseases.Inflammation runs through the pathological process of MIRI.As an important regulator of the body′s defense response,nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome can drive and amplify inflammatory response by activating downstream inflammatory cytokines,and mediate cell and tissue damage,which has been shown to be important in the disease development of MIRI.Selective regulation of NLRP3 inflammasome may provide a new target for the clinical protective treatment of MIRI in the future.