未折叠蛋白反应
自噬
内质网
细胞生物学
细胞内
细胞外
细胞凋亡
功能(生物学)
袋3
蛋白质折叠
化学
ATG5型
ATF6
溶酶体
粒体自噬
蛋白质稳态
程序性细胞死亡
自噬体
ATG16L1
生物
生物化学
作者
W. S. Lee,Wan Hee Yoo,Han-Jung Chae
出处
期刊:Current Molecular Medicine
[Bentham Science]
日期:2015-10-06
卷期号:15 (8): 735-745
被引量:156
标识
DOI:10.2174/1566524015666150921105453
摘要
Eukaryotic cells respond to various types of stresses caused by changes in the extracellular environment. Intracellular factors, such as the accumulation of misfolded proteins in the endoplasmic reticulum (ER), also cause stress and activate the unfolded protein response (UPR), which induces the expression of chaperones and proteins involved in the recovery process. However, if the stress is excessive or sustained, and ER function cannot be restored, the UPR triggers apoptosis, thereby removing the affected cell. It is now apparent that ER stress is also a potent trigger for autophagy, a self-degradative process that has an adaptive function. This review surveys the intersection of ER stress and autophagy and highlights the potential therapeutic implications thereof.
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