期刊
FRONTIERS IN CELLULAR NEUROSCIENCE
卷 16, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fncel.2022.864426
关键词
ER stress; unfolded protein response (UPR); cerebral ischemia-reperfusion injury (CIRI); inflammation; apoptosis
资金
- Fundamental Research Funds for the Central Universities [2042020kf0079]
- Health Commission of Hubei Province Scientific Research Project [WJ2021M148]
- National Natural Science Foundation of China [82171336, 81870939, 82071339, 81771283]
- Hubei Province Key Laboratory Open Project [2021KFY044]
Ischemic stroke is a cerebrovascular disease that can lead to severe disability and death. Current treatment methods for ischemic stroke are limited and have a narrow treatment window. Recovery of cerebral blood flow causes cerebral ischemia/reperfusion injury, in which endoplasmic reticulum stress plays a crucial role.
Ischemic stroke is an acute cerebrovascular disease characterized by sudden interruption of blood flow in a certain part of the brain, leading to serious disability and death. At present, treatment methods for ischemic stroke are limited to thrombolysis or thrombus removal, but the treatment window is very narrow. However, recovery of cerebral blood circulation further causes cerebral ischemia/reperfusion injury (CIRI). The endoplasmic reticulum (ER) plays an important role in protein secretion, membrane protein folding, transportation, and maintenance of intracellular calcium homeostasis. Endoplasmic reticulum stress (ERS) plays a crucial role in cerebral ischemia pathophysiology. Mild ERS helps improve cell tolerance and restore cell homeostasis; however, excessive or long-term ERS causes apoptotic pathway activation. Specifically, the protein kinase R-like endoplasmic reticulum kinase (PERK), activating transcription factor 6 (ATF6), and inositol-requiring enzyme 1 (IRE1) pathways are significantly activated following initiation of the unfolded protein response (UPR). CIRI-induced apoptosis leads to nerve cell death, which ultimately aggravates neurological deficits in patients. Therefore, it is necessary and important to comprehensively explore the mechanism of ERS in CIRI to identify methods for preserving brain cells and neuronal function after ischemia.
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