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内质网应激与心脏代谢疾病。

Endoplasmic reticulum stress in cardiometabolic disorders.

机构信息

Department of Medicine, Columbia University, New York, NY 10032, USA.

出版信息

Curr Atheroscler Rep. 2012 Oct;14(5):469-75. doi: 10.1007/s11883-012-0270-z.

Abstract

When endoplasmic reticulum (ER) homeostasis is disrupted, an adaptive signaling pathway, called the unfolded protein response (UPR) is activated to help ER cope with the stress. The UPR is an important signal transduction pathway, crucial for the survival and function of all cells. Recently, there has been a substantial progress made in understanding the molecular mechanisms of physiological UPR regulation and its role in the pathogenesis of many diseases including metabolic diseases. Studies using mouse models lacking or overexpressing the factors involved in ER stress signaling as well as work performed on humans have revealed the contribution of UPR to disease progression. This review focuses on the regulation of UPR signaling and its relevance in pathogenesis of metabolic diseases.

摘要

当内质网(ER)稳态被破坏时,一种称为未折叠蛋白反应(UPR)的适应性信号通路被激活,以帮助 ER 应对应激。UPR 是一种重要的信号转导途径,对所有细胞的存活和功能都至关重要。最近,人们在理解生理 UPR 调节的分子机制及其在包括代谢疾病在内的许多疾病发病机制中的作用方面取得了重大进展。使用缺乏或过表达 ER 应激信号相关因子的小鼠模型进行的研究以及对人类的研究揭示了 UPR 对疾病进展的贡献。本综述重点介绍了 UPR 信号的调节及其在代谢性疾病发病机制中的相关性。

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