防治血管再狭窄的新靶点——缝隙连接蛋白43  

Connexin43:a new potential therapeutic target in restenosis

作　　者：朱玲玉[1] 蒋丽萍[1] 

机构地区：[1]南昌大学医学院药理教研室,江西南昌330006

出　　处：《中国新药与临床杂志》2008年第6期446-449,共4页Chinese Journal of New Drugs and Clinical Remedies

基　　金：国家自然科学基金(30760286)

摘　　要：缝隙连接是介导相邻细胞间离子和小分子信号物质直接交换的跨膜通道,血管平滑肌细胞中主要表达连接蛋白43(connexin43,CX43)。研究表明,CX43表达上调与平滑肌细胞的增殖、迁移及细胞外基质生成密切相关,促使血管损伤后新内膜生成,引起血管再狭窄,提示CX43可能成为血管性疾病治疗的新靶点。本文综述CX43与血管再狭窄之间关系及以CX43为靶点的药物和基因治疗的研究进展。Gap junctions are clusters of transmembrane channels that mediate direct exchange of ions and small signaling molecules between adjacent ceils. The major gap junction protein expressed in vascular smooth muscle cells （VSMCs） is connexin43 （CX43） . Upregulation of CX43 is closely associated with migration, proliferation of VSMCs and synthesis of extracellular matrix, which lead to neointimal formation after vascular injury, and result in the development of restenosis. Studies suggested that CX43 might be a new target for treating restenosis. The relationship between CX43 and restenosis and advances in the study of new therapy strategies based on CX43 were reviewed in this article.

关 键 词：连接蛋白43 冠状动脉再狭窄 基因疗法 缝隙连接 

分 类 号：R541.4[医药卫生—心血管疾病] R972[医药卫生—内科学]