Matrix metalloproteinases: A therapeutic target in cardiovascular disease

被引:57
作者
Sierevogel, MJ
Pasterkamp, G
de Kleijn, DPV
Strauss, BH
机构
[1] Univ Utrecht, Ctr Med, Expt Cardiol Lab, Dept Cardiol, NL-3584 CX Utrecht, Netherlands
[2] St Michaels Hosp, Terrence Donnelly Heart Ctr, Roy & Ann Foss Intervent Res Program, Toronto, ON, Canada
关键词
MMPs; MMP inhibitors; extracellular matrix turnover; de novo atherosclerotic plaque destabilization; arterial remodeling; restenosis; aneurysm formation; heart failure;
D O I
10.2174/1381612033455099
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Cardiovascular disease is the leading cause of death in Western society. Extracellular matrix turnover is L important in many cardiovascular pathologies, such as arterial remodeling. plaque rupture, restenosis, aneurysm formation and heart failure. Matrix metalloproteinases (MMPs) belong to a group of zinc and calcium dependent proteases and cause breakdown of the extracellular matrix. MMP inhibitors have been developed and tested for their effect on the outcome of oncological disease [1]. Recent preclinical research revealed that these MMP inhibitors could also have great potential in the field of cardiovascular disease. This preclinical research has encouraged investigators to design and start the First clinical studies with cardiovascular endpoints. In the present paper, the various aspects of MMP participation in cardiovascular disease will be summarized. Preclinical demonstrated the effect and potential of applicable MMP inhibitors on different cardiovascular disease animal studies that entities will be discussed. We Will specifically focus Oil the role of MMPs and the potential of their inhibitors in de novo remodeling, restenosis after ballon angioplasty and stenting, aneurysm atherosclerotic plaque destabilization, arterial formation and heart failure. We Conclude that MMP inhibitors are likely to be useful in the development of pharmacological approaches to reduce cardiovascular death. considering file positive Outcomes after usage of MMP inhibitors in restenosis and arterial remodeling.
引用
收藏
页码:1033 / 1040
页数:8
相关论文
共 100 条
[51]   Histopathologic comparison of human coronary instent and post-balloon angioplasty restenotic tissue [J].
Moreno, PR ;
Palacios, IF ;
Leon, MN ;
Rhodes, J ;
Fuster, V ;
Fallon, JT .
AMERICAN JOURNAL OF CARDIOLOGY, 1999, 84 (04) :462-+
[52]   MATRIX METALLOPROTEINASES IN ABDOMINAL AORTIC-ANEURYSM - CHARACTERIZATION PURIFICATION, AND THEIR POSSIBLE SOURCES [J].
NEWMAN, KM ;
MALON, AM ;
SHIN, RD ;
SCHOLES, JV ;
RAMEY, WG ;
TILSON, MD .
CONNECTIVE TISSUE RESEARCH, 1994, 30 (04) :265-276
[53]   Contribution of inadequate compensatory enlargement to development of human coronary artery stenosis: An in vivo intravascular ultrasound study [J].
Nishioka, T ;
Luo, H ;
Eigler, NL ;
Berglund, H ;
Kim, CJ ;
Siegel, RJ .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 1996, 27 (07) :1571-1576
[54]   The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely within the arterial system - A postmortem study [J].
Pasterkamp, G ;
Schoneveld, AH ;
vanWolferen, W ;
Hillen, B ;
Clarijs, RJG ;
Haudenschild, CC ;
Borst, C .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1997, 17 (11) :3057-3063
[55]   Arterial remodeling in atherosclerosis, restenosis and after alteration of blood flow: potential mechanisms and clinical implications [J].
Pasterkamp, G ;
de Kleijn, DPV ;
Borst, C .
CARDIOVASCULAR RESEARCH, 2000, 45 (04) :843-852
[56]   Atherosclerotic arterial remodeling and the localization of macrophages and matrix metalloproteases 1, 2 and 9 in the human coronary artery [J].
Pasterkamp, G ;
Schoneveld, AH ;
Hijnen, DJ ;
de Kleijn, DPV ;
Teepen, H ;
van der Wal, AC ;
Borst, C .
ATHEROSCLEROSIS, 2000, 150 (02) :245-253
[57]   PARADOXICAL ARTERIAL-WALL SHRINKAGE MAY CONTRIBUTE TO LUMINAL NARROWING OF HUMAN ATHEROSCLEROTIC FEMORAL ARTERIES [J].
PASTERKAMP, G ;
WENSING, PJW ;
POST, MJ ;
HILLEN, B ;
MALI, WPTM ;
BORST, C .
CIRCULATION, 1995, 91 (05) :1444-1449
[58]   Medical imaging techniques in the evaluation of strategies for therapeutic angiogenesis [J].
Pearlman, JD ;
Laham, RJ ;
Post, M ;
Leiner, T ;
Simons, M .
CURRENT PHARMACEUTICAL DESIGN, 2002, 8 (16) :1467-1496
[59]   Inhibitors of leukotriene A4 (LTA4) hydrolase as potential anti-inflammatory agents [J].
Penning, TD .
CURRENT PHARMACEUTICAL DESIGN, 2001, 7 (03) :163-179
[60]   Functional polymorphism in the matrix metalloproteinase-9 promoter as a potential risk factor for intracranial aneurysm [J].
Peters, DG ;
Kassam, A ;
Jean, PLS ;
Yonas, H ;
Ferrell, RE .
STROKE, 1999, 30 (12) :2612-2616