病毒性心肌炎与细胞凋亡、缝隙连接蛋白的研究进展  

The research progress between apoptosis,connexin and viral myoearditis

作　　者：黄侠[1] 于影[1] 赵明[1] 

机构地区：[1]内蒙古民族大学附属医院心内科,内蒙古通辽028000

出　　处：《临床心血管病杂志》2016年第7期742-744,共3页Journal of Clinical Cardiology

基　　金：国家自然科学基金课题(No:81360587);内蒙古自治区自然科学基金项目(No:2014MS0898)

摘　　要：病毒性心肌炎(VMC)是一种由各种病毒引起的自身免疫性疾病,其中以柯莎奇B组病毒(CVB)导致的VMC最为常见。VMC容易导致心力衰竭、心律失常等并发症,也是心源性猝死的原因之一。VMC心肌组织中存在明显的细胞凋亡和缝隙连接蛋白变化,细胞凋亡和缝隙连接蛋白可能参与了VMC的发生和发展,在其发病机制中起重要作用。Viral myocarditis（VMC）is a kind of autoimmune disease,which be induced by all kinds of virus,especially by Coxsackievirus B（CVB）.It can lead to some complication,such as heart failure,arrhythmia and so on.Also it is one cause of sudden cardiac death.Recently,the study had found that the obvious apoptosis and significant change of connexin existed in myocardial tissue with VMC,suggesting that the apoptosis and connexin play an important role in pathogenesis of VMC and participate in the occurrence and development of VMC.

关 键 词：细胞凋亡 缝隙连接蛋白 病毒性心肌炎 

分 类 号：R541.7[医药卫生—心血管疾病]