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|本期目录/Table of Contents|

内质网应激与糖尿病心肌纤维化

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2014年第1期
页码:
91-93
栏目:
综述
出版日期:
2013-12-02

文章信息/Info

Title:
Endoplasmic reticulum stress and diabetes mellitus myocardial fibrosis
作者:
杨 琼; 吴永全
（首都医科大学附属北京友谊医院心血管中心，北京 100050）
Author(s):
YANG Qong;  WU Yong-quan
(Cardiovascular Center, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China)
关键词:
内质网应激; 糖尿病; 心肌纤维化
Keywords:
endoplasmic reticulum stress;  diabetes mellitus;  myocardial fibrosis
分类号:
R542.2
DOI:
-
文献标识码:
A
摘要:
内质网（endoplasmic reticulum ER）应激是细胞对缺血、缺氧及高血糖等的一种细胞的适应性反应，其有3条通路，包括双链RNA依赖的蛋白激酶样ER激酶(PKR-like ER kinase,PERK)、肌醇依赖酶1α(inositol-requiring enzyme 1,IRE-1α,又称核酸内切酶)与激活转录因子6(activating transcription factor 6,ATF6)。而过度的ER应激可通过CHOP、JNK、半胱氨酸天冬氨酸特异性蛋白酶(caspase)途径引起细胞凋亡，如果是在糖尿病(DM)患者则可以刺激心肌间质成纤维细胞，引起心肌重构、胶原沉积。近年来，越来越多的研究表明，DM心肌纤维化与ER应激有关，其机制的研究对于开发研制靶作用的药物非常重要。本文将对目前关于ER应激的作用途径以及DM心肌纤维化的机制做简要介绍。
Abstract:
Endoplasmic reticulum (ER) stress is a type of cellular adaptive reaction to ischemia, hypoxia and hyperglycemia and has three pathways, namely, PKR-like ER kinase (PERK), inositol-requiring enzyme 1 (IRE-1α) and activating transcription factor 6 (ATF6). Strong ER stress will induce cellular apoptosis through CHOP, JNK and caspase pathways, which may stimulate myocardial interstitial fibroblast and result in myocardial remodeling and collagen deposition. In recent years, many studies show that diabetes mellitus (DM) myocardial fibrosis has a close relation to ER stress and a better understanding of the mechanism between them is important for the development of new drugs for DM myocardial fibrosis. In this article we will introduce the mechanism and pathways of ER stress and the mechanism of DM myocardial fibrosis and look into the possible relation between the two.

参考文献/References

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备注/Memo

备注/Memo:
收稿日期：2013-04-26.通讯作者：吴永全，主任医师， 主要从事心律失常和心脏病介入研究 Email：wuyongquan67@126.com 作者简介：杨琼，硕士生 Email：yangqiong19901005@126.com
更新日期/Last Update: 2014-01-20