ER Stress and Autophagy
ER Stress and Autophagy
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DOI：
10.2174/1566524015666150921105453
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发表时间：
2015-01-01
影响因子：
2.5
通讯作者：
Chae, H. -J.
中科院分区：
文献类型：
--
作者：
Lee, W. -S.;Yoo, W. -H.;Chae, H. -J.
真核细胞对细胞外环境变化引起的各种压力做出反应。细胞内因素，例如内质网 (ER) 中错误折叠蛋白的积累，也会引起应激并激活未折叠蛋白反应 (UPR)，从而诱导参与恢复过程的伴侣和蛋白的表达。然而，如果压力过度或持续，并且ER功能无法恢复，UPR就会触发细胞凋亡，从而清除受影响的细胞。现在很明显，内质网应激也是自噬的有效触发因素，自噬是一种具有适应性功能的自我降解过程。这篇综述调查了内质网应激和自噬的交叉点，并强调了其潜在的治疗意义。
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.