NLRP3炎症小体与线粒体功能障碍在脓毒性心肌病发病机制中的交互作用
Interaction between NOD-like receptor protein 3 inflammatory corpuscles and mitochondrial dysfunction in the pathogenesis of septic cardiomyopathy
袁玉凡 1沈琪 1晋金兰1
作者信息
- 1. 广州中医药大学深圳医院(福田)重症医学科,广东深圳 518034
- 折叠
摘要
脓毒性心肌病(SCM)发病率高且发病机制复杂,会显著增加脓毒症患者病死率.NOD样受体蛋白 3(NLRP3)炎症小体在SCM发病机制中起重要作用,心肌细胞线粒体功能障碍亦是SCM的重要发病机制之一,NLRP3 炎症小体激活与线粒体功能障碍密切相关,研究二者之间的交互作用机制有助于寻找SCM新的治疗方案.本文就NLRP3 炎症小体与线粒体功能障碍在SCM发病机制中的交互作用及中医药防治SCM的相关机制进行综述,为深入探究SCM的治疗靶点提供理论参考依据.
Abstract
Septic cardiomyopathy(SCM)has a high incidence and complex pathogenesis,which can significantly increase the mortality of sepsis patients.NOD-like receptor protein 3(NLRP3)inflammatory corpuscles play an important role in the pathogenesis of SCM.Mitochondrial dysfunction in cardiomyocytes is also one of the important pathogenesis of SCM.Activation of NLRP3 inflammatory corpuscles is closely related to mitochondrial dysfunction.The study of interaction mechanism between the two is helpful to find a new therapeutic scheme for SCM.This article reviews the interaction between NLRP3 inflammatory corpuscles and mitochondrial dysfunction in the pathogenesis of SCM,as well as the related mechanisms of traditional Chinese medicine(TCM)prevention and treatment of SCM,providing theoretical reference for further exploring therapeutic targets for SCM.
关键词
脓毒性心肌病/NOD样受体蛋白3/线粒体功能障碍/交互作用Key words
Septic cardiomyopathy/NOD-like receptor protein 3/Mitochondrial dysfunction/Interaction引用本文复制引用
基金项目
国家自然科学基金(82274288)
广东省自然科学基金(2022A1515011641)
深圳市科技计划(JCYJ20210324121808024)
深圳市科技计划(JCYJ20190809111013327)
出版年
2024
NETL
NSTL
万方数据