Mitochondria ROS and mitophagy in acute kidney injury

被引:421
作者
Su, Lianjiu [1 ,2 ]
Zhang, Jiahao [1 ]
Gomez, Hernando [3 ]
Kellum, John A. [3 ]
Peng, Zhiyong [1 ,3 ]
机构
[1] Wuhan Univ, Dept Crit Care Med, Zhongnan Hosp, 169 Donghu Rd, Wuhan 430071, Hubei, Peoples R China
[2] NCI, Ctr Canc Res, Neurooncol, NIH, Bethesda, MD USA
[3] Univ Pittsburgh, Dept Crit Care Med, Ctr Crit Care Nephrol, Med Ctr, Pittsburgh, PA USA
基金
中国国家自然科学基金;
关键词
Acute kidney injury; cell death; mitochondria; mitophagy; reactive oxygen species; TUBULAR EPITHELIAL-CELLS; PERMEABILITY TRANSITION; INFLAMMASOME ACTIVATION; NADPH OXIDASES; COMPLEX I; BECLIN; AUTOPHAGY; PARKIN; FAMILY; BINDING;
D O I
10.1080/15548627.2022.2084862
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitophagy is an essential mitochondrial quality control mechanism that eliminates damaged mitochondria and the production of reactive oxygen species (ROS). The relationship between mitochondria oxidative stress, ROS production and mitophagy are intimately interwoven, and these processes are all involved in various pathological conditions of acute kidney injury (AKI). The elimination of damaged mitochondria through mitophagy in mammals is a complicated process which involves several pathways. Furthermore, the interplay between mitophagy and different types of cell death, such as apoptosis, pyroptosis and ferroptosis in kidney injury is unclear. Here we will review recent advances in our understanding of the relationship between ROS and mitophagy, the different mitophagy pathways, the relationship between mitophagy and cell death, and the relevance of these processes in the pathogenesis of AKI.
引用
收藏
页码:401 / 414
页数:14
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