血管损伤修复与基质金属蛋白酶  被引量:4

Matrix metalloproteinase and vascular injury repair

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作  者:朱勇锋[1] 司忠义[1] 

机构地区:[1]辽宁医学院附属第一医院心脏大血管外科,辽宁省锦州市121001

出  处:《中国组织工程研究与临床康复》2010年第46期8673-8676,共4页Journal of Clinical Rehabilitative Tissue Engineering Research

摘  要:背景:基质金属蛋白酶是一组能特异降解细胞外基质成分依赖锌的酶家族,近年来研究发现其参与了血管损伤后早期应激反应,与血管损伤后再狭窄发生相关。目的:就基质金属蛋白酶在血管损伤中的一些生理病理过程做一综述。方法:应用计算机检索Medline数据库、Ovid数据库、Springerlink数据库、维普数据库及中国知网数据库,纳入1990/2010发表的29篇基质金属蛋白酶与血管损伤以及药物等干预有关的文献进行总结分析。结果与结论:心血管动脉系统在损伤后,包括经皮腔内血管成形后血管狭窄的发生率较高。基质金属蛋白酶在受损动脉的局部表达增加,通过促进内膜增厚和改变血管重构而促进血管损伤后再狭窄的发生。因此,降低血管受损局部基质金属蛋白酶表达将成为防治血管内再狭窄的一个方向。BACKGROUND:Matrix metalloproteinases(MMPs) are a family of zinc(Zn)-dependent endopeptidases that are collectively capable of cleaving virtually all extracellular matrix substrates.Recently studies demonstrated that MMPs participate in early stress reaction and are closely related to restenosis following vascular injury.OBJECTIVE:To review the physiological and pathological processes of MMPs during vascular injury.METHODS:A compute based online search was performed on Medline,ovid,springerlink,VIP and CNKI,29 documents(1990-2010) related to MMPs and vascular injury or drug intervention were summarized.RESULTS AND CONCLUSION:The ratio of restenosis was very high after the cardiovascular system injured or percutaneous transluminal angioplasty.MMPs expression was increased in local area after vascular injury,which could accelerate restenosis by promoting endometrial thickness and changing vascular remodeling.Therefore,reduction of MMPs expression in the local area after vascular injury provides a direction for preventing and curing vascular restenosis.

关 键 词:血管损伤 血管内再狭窄 基质金属蛋白酶 基质金属蛋白酶组织抑制因子 血管组织工程 

分 类 号:R318[医药卫生—生物医学工程]

 

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