心肌肥厚分子机制研究进展  

Progress in Molecular Mechanisms of Cardiac Hypertrophy

作　　者：戴文建[1] 王以光[1] 

机构地区：[1]中国医学科学院中国协和医科大学医药生物技术研究所,北京100050

出　　处：《心血管病学进展》2009年第1期47-50,共4页Advances in Cardiovascular Diseases

基　　金：国家863课题(2006AA02A307)

摘　　要：心肌肥厚是心脏为适应血流动力学过负荷而发生的增生,它最终将导致心力衰竭,甚至猝死。心肌肥厚是许多心脏疾病发展的一个重要阶段,但是它的形成机制到现在还没有完全清楚。近年研究表明相关的信号通路主要集中在MAPK通路,Ca2+及其依赖的信号转导通路,磷脂酰肌醇-3激酶及其介导的信号转导通路和JAK/STAT信号通路等几条,并且信号通路之间相互联系。Cardiac hypertrophy is a functionally useful adaptation in response to haemodynamie overload. Hypertrophy is associated with an increased rate of sudden deaths. Cardiac hypertrophy is an important phase in heart disease development, but so far its molecular mechanism is not clear. Recent studies indicate that there are several signal pathways related to cardiac hypertrophy, including the mitogenactivated protein kinase pathway, the （ MAPK ） pathways, Ca^2＋ and its dependent signal pathways, phosphoinositide 3-kinase （ PIP3 ） , and its mediated signal pathway, and Janus kinase/signal transducer and activator of transcription signal pathway. Intercommunication was also observed between these signal pathways.

关 键 词：心肌肥厚 分子机制 信号通路 

分 类 号：R541[医药卫生—心血管疾病]