Autophagy and Ischemic Stroke

被引:55
|
作者
Zhang, Yanlin [1 ]
Cao, Yongjun [1 ]
Liu, Chunfeng [1 ]
机构
[1] Soochow Univ, Affiliated Hosp 2, Dept Neurol, Suzhou, Peoples R China
关键词
Ischemic stroke; Autophagy; Apoptosis; Necrosis; Self-adaption; ACTIVATED PROTEIN-KINASE; CELL-DEATH; REPERFUSION INJURY; BRAIN; APOPTOSIS; AGGREGATION; RAPAMYCIN; GROWTH;
D O I
10.1007/978-981-15-4272-5_7
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Ischemic stroke refers to brain tissue ischemia, hypoxic necrosis, and brain softening caused by the interruption of the blood supply to the brain without adequate collateral circulation, thus resulting in neurological symptoms. Autophagy is activated in various cell types in the brain, such as neurons, glial cells, and microvascular cells, upon ischemic stroke. Autophagy efflux injury plays an important role in this pathologic process. This chapter outlines the induction of basal autophagy, autophagy in neurons, and the crosstalk between autophagy, necrosis, and apoptosis that contributes to ischemic stroke. We will highlight the interactions between autophagy, oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction, and the role of autophagy in ischemic stroke. We will also review the recent advances in the understanding of the involvement of autophagy in the pathological process of cerebral ischemic preconditioning, periconditioning, and postconditioning.
引用
收藏
页码:111 / 134
页数:24
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