基质金属蛋白酶与自体移植静脉再狭窄  

Matrix metalloproteinase and autologous vein graft failure

作　　者：何伟[1] 刘志勇[1] 

机构地区：[1]东南大学附属中大医院心胸外科,江苏南京210009

出　　处：《现代医学》2004年第6期414-416,共3页Modern Medical Journal

摘　　要：自体移植静脉再狭窄严重影响冠状动脉旁路移植术远期疗效 ,基质金属蛋白酶 (MMP)是一族细胞外基质降解酶 ,近年来发现它们在自体移植静脉再狭窄过程中发挥了重要作用。自体静脉移植后MMPs的表达及活性增强 ,通过影响基质转换及血管壁细胞功能而促进内膜增生 ,并参与移植静脉收缩性再构。非选择性MMP抑制剂可减轻内膜增生 ,预防移植静脉再狭窄。Failure of coronary artery venous grafts occurs at a substantial rate and has a large impact on the long-term effect of the operation of coronary artery bypass grafting. Matrix metalloproteinases are the family of highly regulated peptidases that are collectively responsible for the degradation of extracellular matrix.In recent years, MMP are thought to play an important role in the process of vein graft failure.Increased MMP expression and activity have been identified after vein grafted into artery system. Through mechanisms that rely on degradation and reorganization of extracellular matrix,MMP contributes to intimal hyperplasia as well as constractive remodeling in the vein graft.Use of nonspecific inhibitors can decrease intimal thickening and seems to prevent vein graft stenosis.

关 键 词：再狭窄 自体移植静脉 基质金属蛋白酶 MMP 内膜增生 血管壁细胞 自体静脉移植 参与 重要作用 过程 

分 类 号：R654[医药卫生—外科学] R543[医药卫生—临床医学]