Matrix metalloproteinases in critical limb ischemia

被引：13
作者：
Hobeika, Mark J. [1 ]
Edlin, Rachel S. [1 ]
Muhs, Bart E. [1 ]
Sadek, Mikel [1 ]
Gagne, Paul J. [1 ]
机构：
[1] NYU, Dept Surg, Sch Med, New York, NY 10016 USA
来源：
JOURNAL OF SURGICAL RESEARCH | 2008年 / 149卷 / 01期
关键词：
matrix metalloproteinases; critical limb ischemia; atherosclerosis; angiogenesis; arteriogenesis;
D O I：
10.1016/j.jss.2007.08.004
中图分类号：
R61 [外科手术学];
学科分类号：
摘要：
Critical limb ischemia (CLI) is most commonly the result of arterial occlusive disease, specifically atherosclerotic plaque formation and rupture within the infrainguinal arteries. The physiological response to CLI is partial limb reperfusion via the distinct processes of angiogenesis and arteriogenesis. Matrix metalloproteinases (MMPs) are extracellular matrix-remodeling enzymes that play an important role in both the occlusion and reperfusion processes associated with CLI. This article provides a review of the recent literature, summarizing the current understanding of the role of MMPs in both the arterial occlusion and limb reperfusion associated with CLI. Specifically, the functions of MMPs in atherosclerosis, angiogenesis, and arteriogenesis are discussed. (c) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码：148 / 154
页数：7
相关论文
共 65 条
[1]   Serum values of metalloproteinase-2 and metalloproteinase-9 as related to unstable plaque and inflammatory cells in patients with greater than 70% carotid artery stenosis [J].
Alvarez, B ;
Ruiz, C ;
Chacón, P ;
Alvarez-Sabin, J ;
Matas, M .
JOURNAL OF VASCULAR SURGERY, 2004, 40 (03) :469-475
[2]  
Amorino GP, 1998, AM J PATHOL, V152, P199
[3]   Critical issues in peripheral arterial disease detection and management - A call to action [J].
Belch, JJF ;
Topol, EJ ;
Agnelli, G ;
Bertrand, M ;
Califf, RM ;
Clement, DL ;
Creager, MA ;
Easton, JD ;
Gavin, JR ;
Greenland, P ;
Hankey, G ;
Hanrath, P ;
Hirsch, AT ;
Meyer, J ;
Smith, SC ;
Sullivan, F ;
Weber, MA .
ARCHIVES OF INTERNAL MEDICINE, 2003, 163 (08) :884-892
[4]   HMG-CoA reductase inhibitors reduce MMP-9 secretion by macrophages [J].
Bellosta, S ;
Via, D ;
Canavesi, M ;
Pfister, P ;
Fumagalli, R ;
Paoletti, R ;
Bernini, F .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1998, 18 (11) :1671-1678
[5]   Matrix metalloproteinase-9 triggers the angiogenic switch during carcinogenesis [J].
Bergers, G ;
Brekken, R ;
McMahon, G ;
Vu, TH ;
Itoh, T ;
Tamaki, K ;
Tanzawa, K ;
Thorpe, P ;
Itohara, S ;
Werb, Z ;
Hanahan, D .
NATURE CELL BIOLOGY, 2000, 2 (10) :737-744
[6]   IDENTIFICATION OF 92-KD GELATINASE IN HUMAN CORONARY ATHEROSCLEROTIC LESIONS - ASSOCIATION OF ACTIVE ENZYME-SYNTHESIS WITH UNSTABLE ANGINA [J].
BROWN, DL ;
HIBBS, MS ;
KEARNEY, M ;
LOUSHIN, C ;
ISNER, JM .
CIRCULATION, 1995, 91 (08) :2125-2131
[7]   Remodeling of the vascular tunica media is essential for development of collateral vessels in the canine heart [J].
Cai, WJ ;
Kocsis, E ;
Wu, XQ ;
Rodríguez, M ;
Luo, XG ;
Schaper, W ;
Schaper, J .
MOLECULAR AND CELLULAR BIOCHEMISTRY, 2004, 264 (1-2) :201-210
[8]   Remodeling of the adventitia during coronary arteriogenesis [J].
Cai, WJ ;
Koltai, S ;
Kocsis, E ;
Scholz, D ;
Kostin, S ;
Luo, XG ;
Schaper, W ;
Schaper, J .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2003, 284 (01) :H31-H40
[9]   Mechanisms of angiogenesis and arteriogenesis [J].
Carmeliet, P .
NATURE MEDICINE, 2000, 6 (04) :389-395
[10]   Matrix metalloproteinase-9 is necessary for the regulation of smooth muscle cell replication and migration after arterial injury [J].
Cho, A ;
Reidy, MA .
CIRCULATION RESEARCH, 2002, 91 (09) :845-851
1234567