Endoplasmic reticulum stress in brain ischemia

被引:58
作者
Su, Yingchao [1 ]
Li, Feng [1 ]
机构
[1] Harbin Med Univ, Affiliated Hosp 2, Dept Neurol, Harbin 150086, Heilongjiang Pr, Peoples R China
关键词
brain ischemia; endoplasmic reticulum stress; UNFOLDED PROTEIN RESPONSE; ER-ASSOCIATED DEGRADATION; RYANODINE RECEPTOR; CEREBRAL-ISCHEMIA; NA+/CA2+ EXCHANGER; SIGNALING PATHWAY; INDUCED AUTOPHAGY; CA2+ HOMEOSTASIS; GENE-EXPRESSION; DOWN-REGULATION;
D O I
10.3109/00207454.2015.1059836
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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.
引用
收藏
页码:681 / 691
页数:11
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