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内质网应激与心肌肥大

刘秀华^*

中国人民解放军总医院病理生理学研究室，北京 100853

摘要

肌浆网是调控心肌细胞钙稳态、蛋白质合成和细胞凋亡的重要亚细胞器。内质网应激是指内质网理化环境改变和过负荷等因素导致未折叠/ 误折叠蛋白在内质网聚集和钙稳态失衡等内质网功能紊乱状态。适度的内质网应激有利于心肌细胞代偿，持续而严重的内质网应激则触发内质网应激相关细胞凋亡，造成肥大心肌由代偿转向衰竭，是影响心肌肥大发生、发展的重要因素。本文综述了内质网应激反应在心肌肥大发生、发展中的作用。

关键词： 内质网应激; 心肌肥大; 机制

分类号：R363.2

[Endoplasmic reticulum stress and myocardial hypertrophy.] [Ariticle in Chinese]

LIU Xiu-Hua^*

Department of Pathophysiology, Chinese PLA General Hospital, Beijing 100853, China

Abstract

Sarcoplasmic reticulum is a principal subcellular organelle which regulates calcium homeostasis, protein synthesis, and apoptosis of cardiomyocytes. Endoplasmic reticulum (ER) stress is defined as the perturbation of ER function which is caused by the alterations in the ER environment, such as the perturbation of Ca2+ homeostasis, elevated protein synthesis, the deprivation of glucose, altered glycosylation, and the accumulation of misfolded proteins. Moderate ER stress is able to restore cellular homeostasis, i.e., to exert a compensatory effect on cardiomyocytes. However, intense or persistent ER stress may cause ER stress-induced apoptosis, which shifts the hypertrophied myocardium to failure, and affects the pathogenesis and development of myocardial hypertrophy. The article reviewed the role of ER stress response in the pathogenesis and development of myocardial hypertrophy.

Key words: stress; endoplasmic reticulum; cardiac hypertrophy

收稿日期：2008-10-10　　录用日期：2008-12-01

通讯作者：刘秀华　　E-mail: xiuhualiu98@yahoo.com.cn

引用本文：

刘秀华. 内质网应激与心肌肥大[J]. 生理学报 2009; 61 (1): 9-14.

LIU Xiu-Hua. [Endoplasmic reticulum stress and myocardial hypertrophy.] [Ariticle in Chinese] . Acta Physiol Sin 2009; 61 (1): 9-14 (in Chinese with English abstract).