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The binary switch that controls the life and death decisions of ER stressed beta cells

机译:控制ER应激β细胞生死决定的二进制开关

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摘要

Diabetes mellitus is a group of common metabolic disorders defined by hyperglycemia. One of the most important factors contributing to hyperglycemia is dysfunction and death of p cells. Increasing experimental, clinica, and genetic evidence indicates that endoplasmic reticulum (ER) stress plays an important role in beta cell dysfunction and death during the progression of type 1 and type 2 diabetes as well as genetic forms of diabetes such as Wolfram syndrome. The mechanisms of ER stress-mediated beta cell dysfunction and death are complex and not homogenous. Here we review the recent key findings on the role of ER stress and the unfolded protein response (UPR) in beta cells and the mechanisms of ER stress-mediated beta cell dysfunction and death. Complete understanding of those mechanisms will lead to novel therapeutic modalities for diabetes.
机译:糖尿病是由高血糖症定义的一组常见的代谢疾病。促成高血糖的最重要因素之一是p细胞功能障碍和死亡。越来越多的实验,临床和遗传证据表明,内质网(ER)应激在1型和2型糖尿病以及糖尿病的遗传形式(例如Wolfram综合征)的进展中,在β细胞功能异常和死亡中起着重要作用。内质网应激介导的β细胞功能障碍和死亡的机制很复杂,而且不均一。在这里,我们回顾最近有关ER应激和未折叠的蛋白反应(UPR)在β细胞中的作用以及ER应激介导的β细胞功能障碍和死亡的机制的关键发现。对这些机制的完全理解将导致糖尿病的新型治疗方式。

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