自噬
串扰
缺血
医学
细胞生物学
内质网
细胞凋亡
冲程(发动机)
神经科学
脑缺血
程序性细胞死亡
心脏病学
病理
生物
生物化学
工程类
物理
光学
机械工程
作者
Yanlin Zhang,Yongjun Cao,Chun‐Feng Liu
标识
DOI:10.1007/978-981-15-4272-5_7
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.
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