基质金属蛋白酶在心肌缺血再灌注损伤中的作用

被引:4
作者
黄健男
张瑞岩
机构
[1] 上海交通大学医学院附属瑞金医院
关键词
基质金属蛋白酶; 缺血再灌注; 心肌损伤;
D O I
10.13241/j.cnki.pmb.2011.13.020
中图分类号
R542.22 [];
学科分类号
1002 ; 100201 ;
摘要
肌缺血再灌注损伤是指缺血心肌组织在恢复血流供给后,其细胞代谢功能障碍及结构破坏反而加重的现象,主要表现在心肌收缩与舒张功能障碍、血管内皮功能障碍、微循环血流紊乱、细胞代谢失调、电解质平衡紊乱、细胞凋亡与坏死等,并伴随着氧自由基的大量产生和毒性损伤以及炎症反应的激活,是一个极其复杂的病理过程。基质金属蛋白酶(MMPs)及其组织抑制物(TIMPs)是心肌组织中多种细胞分泌的内源性细胞因子,其作用涵盖了细胞外基质降解、炎症反应激活、调节血管功能、影响细胞凋亡与存活等众多病理生理过程,而这些过程均在心肌缺血再灌注损伤中发挥着重要的作用。
引用
收藏
页码:2584 / 2586
页数:3
相关论文
共 32 条
[1]  
Infiammation,ProinfammatoryMediators and Myocardial Ischemia reperfusion Injury. Jakob VJ,Rong J,James G,et al. HematolOncol Clin N Am . 2007
[2]  
Myocardial matrix remodeling and the matrixmetalloproteinases:infuence on cardiac form and function. Spinale FG. Physiological Reviews . 2007
[3]  
Combination of tumor necrosis factor-alpha ablation and matrix metalloproteinase inhibition prevents heart failure after pressure overload in tissue inhibitor of metalloproteinase-3 knock-out mice. Kassiri Z,Oudit GY,Sanchez , et al. Circulation Research . 2005
[4]  
Relevance of matrix metalloproteinases and their inhibitors after myocardial infarction: a temporal and spatial window. Vanhoutte D,Schellings M,Pinto Y,Heymans S. Cardiovascular Research . 2006
[5]  
Cardiacfbroblasts:at the heart of myocardialremodeling. Porter KE,Turner NA. Pharmacology and Therapeutics . 2009
[6]  
Signaling pathways in ischemic preconditioning[J] . James M. Downey,Amanda M. Davis,Michael V. Cohen. &nbspHeart Failure Reviews . 2007 (3)
[7]  
Matrix Metalloproteinase-7 Affects Connexin-43 Levels, Electrical Conduction, and Survival After Myocardial Infarction[J] . Merry L. Lindsey,G Patricia Escobar,Rupak Mukherjee,Danielle K. Goshorn,Nina J. Sheats,James A. Bruce,I Matthew Mains,Jennifer K. Hendrick,Kenneth W. Hewett,Robert G. Gourdie,Lynn M. Matrisian,Francis G. Spinale. &nbspCirculation . 2006 (25)
[8]   Combination of tumor necrosis factor-α ablation and matrix metalloproteinase inhibition prevents heart failure after pressure overload in tissue inhibitor of metalloproteinase-3 knock-out mice [J].
Kassiri, Z ;
Oudit, GY ;
Sanchez, O ;
Dawood, F ;
Mohammed, FF ;
Nuttall, RK ;
Edwards, DR ;
Liu, PP ;
Backx, PH ;
Khokha, R .
CIRCULATION RESEARCH, 2005, 97 (04) :380-390
[9]   Loss or inhibition of uPA or MMP-9 attenuates LV remodeling and dysfunction after acute pressure overload in mice [J].
Heymans, S ;
Lupu, F ;
Terclavers, S ;
Vanwetswinkel, B ;
Herbert, JM ;
Baker, A ;
Collen, D ;
Carmeliet, P ;
Moons, L .
AMERICAN JOURNAL OF PATHOLOGY, 2005, 166 (01) :15-25
[10]  
TIMP-3 deficiency accelerates cardiac remodeling after myocardial infarction. Tian H,Cimini M,Fedak PW,et al. Journal of Molecular and Cellular Cardiology . 2007