Endoplasmic reticulum stress in beta-cells and development of diabetes.
Endoplasmic reticulum stress in beta-cells and development of diabetes.
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DOI：
10.1016/j.coph.2009.07.003
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发表时间：
2009-12
影响因子：
4
通讯作者：
Urano, Fumihiko
中科院分区：
文献类型：
--
作者：
Fonseca, Sonya G.;Burcin, Mark;Gromada, Jesper;Urano, Fumihiko
内质网（ER）是负责多种重要细胞功能的细胞区室，包括用于分泌的新合成蛋白质（如胰岛素）的生物合成和折叠。许多病理和生理因素干扰ER功能，导致ER稳态失调，导致ER应激。内质网应激激发了一个信号级联反应来缓解应激，即未折叠蛋白反应（UPR）。只要UPR能缓解应激，细胞就能产生适量的蛋白质，维持ER稳态。然而，如果UPR不能维持ER稳态，细胞将经历凋亡。UPR的激活对于具有高分泌蛋白产生的胰岛素产生胰腺β细胞的存活至关重要。β细胞中ER稳态的任何破坏都可能导致细胞死亡并有助于糖尿病的发病机制。有几种ER应激介导的糖尿病模型。本文综述了糖尿病进展过程中内质网应激介导的β细胞功能障碍和死亡的分子机制。
The endoplasmic reticulum (ER) is a cellular compartment responsible for multiple important cellular functions including the biosynthesis and folding of newly synthesized proteins destined for secretion, such as insulin. A myriad of pathological and physiological factors perturb ER function and cause dysregulation of ER homeostasis, leading to ER stress. ER stress elicits a signaling cascade to mitigate stress, the Unfolded Protein Response (UPR). As long as the UPR can relieve stress, cells can produce the proper amount of proteins and maintain ER homeostasis. If the UPR, however, fails to maintain ER homeostasis, cells will undergo apoptosis. Activation of the UPR is critical to the survival of insulin-producing pancreatic β-cells with high secretory protein production. Any disruption of ER homeostasis in β-cells can lead to cell death and contribute to the pathogenesis of diabetes. There are several models of ER stress-mediated diabetes. In this review, we outline the underlying molecular mechanisms of ER stress-mediated β-cell dysfunction and death during the progression of diabetes.
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