Death and survival of neuronal and astrocytic cells in ischemic brain injury： a role of autophagy

Autophagy is a highly regulated cellular mechanism that leads to degradation of long-lived proteins and dysfunctional organelles. The process has been implicated in a variety of physiological and pathological conditions relevant to neurological diseases. Recent studies show the existence of autophag...

Full description

Saved in:
Bibliographic Details
Published in:Acta pharmacologica Sinica 2011-09, Vol.32 (9), p.1089-1099
Main Authors: Xu, Min, Zhang, Hui-ling
Format: Article
Language:English
Subjects:
Animals
Apoptosis
Astrocytes
Astrocytes - cytology
Astrocytes - pathology
Autophagy
Brain - cytology
Brain - pathology
Brain injury
Brain Ischemia - metabolism
Brain Ischemia - pathology
Cell Death
Cell Survival
Endoplasmic reticulum
Humans
Hypoxia
Ischemia
Necrosis
Neurological diseases
Neurons
Neurons - cytology
Neurons - pathology
Organelles
Phagocytosis
Reperfusion
Review
Reviews
再灌注
星形胶质细胞
神经元
神经系统疾病
细胞死亡
缺血性脑损伤
脑缺氧
自噬作用
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Autophagy is a highly regulated cellular mechanism that leads to degradation of long-lived proteins and dysfunctional organelles. The process has been implicated in a variety of physiological and pathological conditions relevant to neurological diseases. Recent studies show the existence of autophagy in cerebral ischemia, but no consensus has yet been reached regarding the functions of autophagy in this condition. This article highlights the activation of autophagy during cerebral ischemia and/or reperfusion, especially in neurons and astrocytes, as well as the role of autophagy in neuronal or astrocytic cell death and survival. We propose that physiological levels of autophagy, presumably caused by mild to modest hypoxia or ischemia, appear to be protective. However, high levels of autophagy caused by severe hypoxia or ischemia and/or reperfusion may cause self-digestion and eventual neuronal and astrocytic cell death. We also discuss that oxidative and endoplasmic reticulum （ER） stresses in cerebral hypoxia or ischemia and/or reperfusion are potent stimuli of autophagy in neurons and astrocytes. In addition, we review the evidence suggesting a considerable overlap between autophagy on one hand, and apoptosis, necrosis and necroptosis on the other hand, in determining the outcomes and final morphol- ogy of damaged neurons and astrocytes.
ISSN:1671-4083
1745-7254
DOI:10.1038/aps.2011.50