Critical hubs of renal ischemia-reperfusion injury: endoplasmic reticulum-mitochondria tethering complexes.
10.1097/CM9.0000000000001091
- Author:
Huan-Huan ZHAO
1
;
Qiu-Xia HAN
1
;
Xiao-Nan DING
1
;
Jing-Yao YAN
2
;
Qi LI
1
;
Dong ZHANG
1
;
Han-Yu ZHU
1
Author Information
1. Department of Nephrology, The First Medical Centre, Chinese People's Liberation Army General Hospital, Chinese People's Liberation Army Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center of Kidney Diseases, Beijing Key Laboratory of Kidney Disease, Beijing 100853, China.
2. Department of Nephrology, Henan Provincial People's Hospital, Zhengzhou University, Zhengzhou, Henan 450000, China.
- Publication Type:Review
- MeSH:
Endoplasmic Reticulum/metabolism*;
Endoplasmic Reticulum Stress;
Humans;
Mitochondria;
Mitochondrial Membranes/metabolism*;
Mitophagy;
Reperfusion Injury/metabolism*
- From:
Chinese Medical Journal
2020;133(21):2599-2609
- CountryChina
- Language:English
-
Abstract:
Mitochondrial injury and endoplasmic reticulum (ER) stress are considered to be the key mechanisms of renal ischemia-reperfusion (I/R) injury. Mitochondria are membrane-bound organelles that form close physical contact with a specific domain of the ER, known as mitochondrial-associated membranes. The close physical contact between them is mainly restrained by ER-mitochondria tethering complexes, which can play an important role in mitochondrial damage, ER stress, lipid homeostasis, and cell death. Several ER-mitochondria tethering complex components are involved in the process of renal I/R injury. A better understanding of the physical and functional interaction between ER and mitochondria is helpful to further clarify the mechanism of renal I/R injury and provide potential therapeutic targets. In this review, we aim to describe the structure of the tethering complex and elucidate its pivotal role in renal I/R injury by summarizing its role in many important mechanisms, such as mitophagy, mitochondrial fission, mitochondrial fusion, apoptosis and necrosis, ER stress, mitochondrial substance transport, and lipid metabolism.
