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脑缺血中的内质网应激

Endoplasmic reticulum stress in brain ischemia.

作者信息

Su Yingchao, Li Feng

机构信息

a Department of Neurology, the Second Affiliated Hospital of Harbin Medical University , Harbin 150086 , China.

出版信息

Int J Neurosci. 2016 Aug;126(8):681-91. doi: 10.3109/00207454.2015.1059836. Epub 2015 Aug 18.

Abstract

Endoplasmic reticulum (ER) stress is an intricate mechanism that mediates numerous responses during brain ischemia, thus being essential to determine the fate of neurons. In recent years, studies of the mechanisms of brain ischemic injury have centered on ER stress, glutamate excitotoxicity, dysfunction of mitochondria, inflammatory reactions, calcium overload and death receptor pathways. The role of ER stress is highly important. In addition to resulting in neuronal cell death through calcium toxicity and apoptotic pathways, ER stress also triggers a series of adaptive responses including unfolded protein response (UPR), autophagy, the expression of pro-survival proteins and the enhancement of ER self-repair ability, leading to less ischemic brain damage. This paper provides an overview of recent advances in understanding of the relations between ER stress and brain ischemia.

摘要

内质网(ER)应激是一种复杂的机制,在脑缺血期间介导多种反应,因此对于决定神经元的命运至关重要。近年来,脑缺血损伤机制的研究集中在内质网应激、谷氨酸兴奋性毒性、线粒体功能障碍、炎症反应、钙超载和死亡受体途径。内质网应激的作用非常重要。除了通过钙毒性和凋亡途径导致神经元细胞死亡外,内质网应激还触发一系列适应性反应,包括未折叠蛋白反应(UPR)、自噬、促生存蛋白的表达以及内质网自我修复能力的增强,从而减少缺血性脑损伤。本文概述了对内质网应激与脑缺血之间关系的最新认识进展。

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