NLRP3炎症小体与相关炎症信号通路在肾缺血-再灌注损伤中的作用  

Role of NLRP3 inflammasome and related inflammatory signaling pathways in renal ischemia-reperfusion injury

作　　者：袁强 申开文 张瑞波 沈俊[1,2] Yuan Qiang;Shen Kaiwen;Zhang Ruibo;Shen Jun(Guizhou Medical University,Guiyang 550004,China;不详)

机构地区：[1]贵州医科大学,贵阳550004 [2]贵州医科大学附属医院泌尿外科

出　　处：《器官移植》2021年第2期177-183,共7页Organ Transplantation

基　　金：贵州省科技计划项目[(2018)5779-6];2020年国家自然科学基金培育项目(贵州医科大学附属医院)[gyfynsfc(2020)-30];贵阳市政府-贵州医科大学联合基金(GY2017-16)。

摘　　要：肾缺血-再灌注损伤(IRI)常见于肾移植术中,是引起急性肾衰竭的重要病理生理过程,严重影响受者预后。炎症反应在IRI的发病机制及病理过程中占据着重要地位。活化的NOD样受体蛋白3(NLRP3)炎症小体可通过介导多种促炎因子的成熟与释放,调节机体炎症反应及相关细胞功能。本文对肾IRI中的NLRP3炎症小体及其相关炎症信号通路的作用机制进行了总结,旨在为临床肾IRI的防治提供新思路。Renal ischemia-reperfusion injury(IRI)commonly occurs in renal transplantation,which is an important pathophysiological process that causes acute renal failure and severely affects clinical prognosis of the recipients.Inflammatory response plays a critical role in the pathogenesis and pathological process of IRI.Activated NOD-like receptor protein 3(NLRP3)inflammasome can mediate the maturation and release of various pro-inflammatory cytokines,thereby regulating the inflammatory response and relevant cell functions.In this article,the mechanism underlying NLRP3 inflammasome and its related inflammatory signaling pathway in renal IRI were reviewed,aiming to provide novel ideas for clinical prevention and treatment of renal IRI.

关 键 词：缺血-再灌注损伤(IRI) 肾移植 NOD样受体蛋白3(NLRP3) Toll样受体(TLR) 模式识别受体(PRR) 半胱氨酸天冬氨酸蛋白酶(Caspase)-1 线粒体DNA(mtDNA) 

分 类 号：R617[医药卫生—外科学]