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。
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 I （IRE-lct） and activating transcription factor 6 （ATF6）. Strong ER stress will induce cellular apoptosis through CHOP, JNK and caspase pathways, which may stimulate myocardial interstitial fibro- blast 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 understand- ing 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.
出处
《心脏杂志》
CAS
2014年第1期91-93,共3页
Chinese Heart Journal
关键词
内质网应激
糖尿病
心肌纤维化
endoplasmic reticulum stress
diabetes mellitus
myocardial fibrosis
