脓毒性心肌病(septic cardiomyopathy,SIC)是脓毒症中常见的器官功能障碍,其与患者高死亡率和不良预后密切相关.SIC发病机制复杂且缺乏有效的治疗手段是亟待解决的关键问题.既往研究表明,线粒体功能障碍在SIC的发生发展中扮演着重要角色.当机体发生SIC导致线粒体功能障碍时,线粒体质量控制系统(mitochondrial quality control system,MQC)的异常调控可使心肌细胞损伤加重.最近的研究显示,MQC可通过调节线粒体生物发生、线粒体融合/裂变和线粒体自噬来维持线粒体动态平衡.因此,本文就MQC在SIC发病中的作用及最新研究进行综述,并对其作为潜在的治疗靶点进行分析与展望.
Progress of research into mitochondrial mass control system's role in the pathogenesis of septic cardiomyopathy
Septic cardiomyopathy(SIC)is an organ dysfunction frequently observed in sepsis and characterized by high mortality and poor prognosis.Understanding the complex pathogenesis of SIC and developing effective therapeutic tools are critical issues that require attention.Previous studies have demonstrated the significant role of mitochondrial dysfunction in the development of SIC.In the presence of SIC,and the mitochondrial dysfunction that result,the aberrant regulation of the mitochondrial quality control system(MQC)can exacerbate cardiomyocyte injury.Recent studies have demonstrated that the MQC maintains the dynamics of mitochondrial homeostasis through its regulation of mitochondrial biogenesis,fusion/fission,and autophagy.This article provides an overview of the role of MQC in SIC pathogenesis,reviews the latest studies in the field,and analyzes MQC's potential as a therapeutic target.
septic cardiomyopathymitochondrial quality control systemmitochondrial biogenesismitochondrial fusion and fissionmitochondrial autophagy