中国组织工程研究

中国组织工程研究 ›› 2010, Vol. 14 ›› Issue (46): 8673-.doi: 10.3969/j.issn.1673-8225.2010.46.030

• 组织构建学术探讨 • 上一篇    下一篇

血管损伤修复与基质金属蛋白酶

朱勇锋，司忠义   

  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
  • 出版日期:2010-11-12 发布日期:2010-11-12
  • 作者简介:朱勇锋★，男，1983年生，河南省项城人，汉族，辽宁医学院在读硕士，主要从事小直径血管的实验研究。 zhuyong127@sohu.com

Matrix metalloproteinase and vascular injury repair

Zhu Yong-feng, Si Zhong-yi   

  1. Department of Cardiovascular Surgery, the First Affiliated Hospital of Liaoning Medical University, Jinzhou  121001, Liaoning Province, China
  • Online:2010-11-12 Published:2010-11-12
  • About author:Zhu Yong-feng★, Studying for master’s degree, Department of Cardiovascular Surgery, the First Affiliated Hospital of Liaoning Medical University, Jinzhou 121001, Liaoning Province, China zhuyong127@sohu.com

PDF

345

被引次数

11

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。

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

Abstract:

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.

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