Endoplasmic reticulum stress in health and disease
Endoplasmic reticulum stress in health and disease
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DOI：
10.1016/j.ceb.2006.06.005
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发表时间：
2006-08-01
影响因子：
7.5
通讯作者：
Ackerman, Susan L.
中科院分区：
文献类型：
--
作者：
Zhao, Lihong;Ackerman, Susan L.
未折叠的蛋白质和其他影响内质网 (ER) 稳态的条件会导致 ER 应激。细胞通过激活未折叠蛋白反应（UPR）来对内质网应激做出反应，这会引起细胞代谢的深刻变化，包括一般翻译减弱、分子伴侣基因的转录上调以及内质网相关降解的激活。然而，长期或急性的内质网应激会导致细胞死亡。最近的进展表明，ER 应激和 UPR 在免疫反应、糖尿病、缺氧条件下的肿瘤生长以及一些神经再生性疾病中发挥着关键作用。对 ER 应激和 UPR 的进一步研究将极大地增强对这些生理和病理过程的理解，并为潜在的治疗提供新的途径。
Unfolded proteins and other conditions affecting endoplasmic reticulum (ER) homeostasis cause ER stress. The cell reacts to ER stress by activation of the unfolded protein response (UPR), which induces profound changes in cellular metabolism including general translation attenuation, transcriptional upregulation of molecular chaperone genes, and activation of ER-associated degradation. However, prolonged or acute ER stress results in cell death. Recent progress suggests that ER stress and UPR play key roles in the immune response, diabetes, tumor growth under hypoxic conditions, and in some neuroclegenerative diseases. Further research on ER stress and UPR will greatly enhance the understanding of these physiological and pathological processes, and provide novel avenues to potential therapies.