Protein Misfolding, Aggregation, and Autophagy After Brain Ischemia

被引：57

作者：

Luo, Tianfei ^{[1
]}

Park, Yujung ^{[1
]}

Sun, Xin ^{[1
]}

Liu, Chunli ^{[1
]}

Hu, Bingren ^{[1
]}

机构：

[1] Univ Maryland, Dept Anesthesiol, Shock Trauma & Anesthesiol Res Ctr, Sch Med, Baltimore, MD 21201 USA

来源：

TRANSLATIONAL STROKE RESEARCH | 2013年 / 4卷 / 06期

关键词：

Brain ischemia; Protein misfolding; Protein aggregation; Autophagy; Protein synthesis; Chaperone; Multiple organelle damage; Ubiquitin-proteasomal system; TRANSIENT CEREBRAL-ISCHEMIA; NUCLEOTIDE EXCHANGE FACTOR; DELAYED NEURONAL DEATH; POSTSYNAPTIC DENSITIES; CELL-DEATH; MOLECULAR CHAPERONES; INHIBITION; MECHANISMS; INJURY; NEURODEGENERATION;

D O I：

10.1007/s12975-013-0299-5

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Ischemic brain injury is a common disorder linked to a variety of diseases. Significant progress has been made in our understanding of the underlying mechanisms. Previous studies show that protein misfolding, aggregation, and multiple organelle damage are major pathological events in postischemic neurons. The autophagy pathway is the chief route for bulk degradation of protein aggregates and damaged organelles. The latest studies suggest that impairment of autophagy contributes to abnormal protein aggregation and organelle damages after brain ischemia. This article reviews recent studies of protein misfolding, aggregation, and impairment of autophagy after brain ischemia.

引用

页码：581 / 588

页数：8

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