Critical hubs of renal ischemia-reperfusion injury: endoplasmic reticulum-mitochondria tethering complexes / 中华医学杂志(英文版)
Chinese Medical Journal
; (24): 2599-2609, 2020.
Article
in En
| WPRIM
| ID: wpr-877854
Responsible library:
WPRO
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.
Full text:
1
Index:
WPRIM
Main subject:
Reperfusion Injury
/
Endoplasmic Reticulum
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Mitochondrial Membranes
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Endoplasmic Reticulum Stress
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Mitophagy
/
Mitochondria
Limits:
Humans
Language:
En
Journal:
Chinese Medical Journal
Year:
2020
Type:
Article