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

VernacularTitle: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
Author: Li MA ¹ ; Haifei SONG ; Guobing CHEN
Author Information

1. 云南省第一人民医院急诊内科/EICU，云南昆明　650032
Keywords: Sepsis; Acute kidney injury; Mitochondrial; Reactive oxygen species; Autophagy
From: Chinese Critical Care Medicine 2022;34(3):317-319
CountryChina
Language:Chinese
Abstract: 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.