线粒体功能障碍在脓毒症相关性急性肾损伤发病机制中的研究进展

Research progress of mitochondrial dysfunction in the pathogenesis of septic acute kidney injury

脓毒症是急性肾损伤(AKI)的常见病因,脓毒症相关性AKI发病机制十分复杂。近年来研究表明,脓毒症患者机体发生氧化应激反应,损伤肾小管上皮细胞中的线粒体,从而诱导细胞死亡;同时,线粒体质量控制受到抑制,包括分裂与融合失衡、自噬过度、合成障碍等加重肾脏损伤。因此,线粒体在脓毒症相关性AKI发病机制中起重要作用,并且可作为脓毒症相关性AKI的潜在治疗靶点。本文就线粒体在脓毒症相关性AKI发病中的作用机制进行综述,探索以线粒体为靶点的脓毒症相关性AKI治疗策略。

Sepsis is a common cause of acute kidney injury(AKI),and the pathogenesis of sepsis-related AKI is very complicated.Recent studies have shown that oxidative stress in septic patients damages mitochondria in renal tubular epithelial cells,and causes cell death.Meanwhile,mitochondrial quality control is inhibited,including imbalance of division and fusion,excessive autophagy,and synthesis disorders,which aggravates kidney injury.Therefore,mitochondria play an important role in the pathogenesis of sepsis-related AKI,and can serve as a potential therapeutic target for sepsis-related AKI.This article reviews the mechanism of mitochondria in the pathogenesis of sepsis-related AKI and explores the treatment strategy by targeting mitochondria.