血管紧张素Ⅱ致心肌纤维化及其信号转导机制研究进展  

Advances in AngⅡ-induced myocardial fi brosis and its signal transduction mechanism

作　　者：谢永进[1] 盖鲁粤[1] 

机构地区：[1]解放军总医院心血管内科,北京100853

出　　处：《解放军医学院学报》2014年第6期630-633,共4页Academic Journal of Chinese PLA Medical School

基　　金：国家自然科学基金项目(30872065)~~

摘　　要：心脏重构包括心脏肥厚和心肌纤维化(myocardial fibrosis,MF)两个方面,MF主要是在各种病理生理因素作用下,心脏局部的成纤维细胞过度增殖,细胞外基质沉积及Ⅰ、Ⅲ型胶原不成比例增加。肾素-血管紧张素-醛固酮系统(reninangiotensin-aldosterone eystem,RAAS)是心肌纤维化过程中重要的神经内分泌机制之一,血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)是RAAS最重要的效应因子,不仅来源于经典的RAAS,还可由心脏局部的心肌细胞和成纤维细胞合成释放,以旁分泌或自分泌的方式发挥生物学效应。AngⅡ致心肌纤维化的信号通路复杂,主要通过与其特异性受体AngⅡ1型受体(angiotensinⅡtype 1 receptor,AT1R)结合,并激活一系列信号分子通路将细胞外信号传递至细胞内产生纤维化效应。Cardiac remodeling includes cardiac hypertrophy and myocardial fibrosis （MF）.MF is mainly manifested as excessive proliferation of local fibroblasts,deposition of extracellular matrix and disproportionate increase of collagens Ⅰ and Ⅲ,under the actions of different pathological and physiological factors.The renin-angiotensin-aldosterone system （RAAS） is one of the most important neuroendocrine mechanisms underlying MF.Ang Ⅱ,derived not only from the classical RAAS,but also from the local cardiac myocytes and fibroblasts,is the most important effect factor of RAAS,who exerts biological effects in a paracrine or autocrine manner.Ang Ⅱ also induces complex signal pathway of MF mainly by binding to its specific AT1R,and activates a series of signal molecular pathways of the extracellular signals into the cells,thus producing fibrosis effect.

关 键 词：血管紧张素Ⅱ 心肌纤维化 信号转导 

分 类 号：R542.23[医药卫生—心血管疾病]