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
[31]   DIFFERENCES IN COMPENSATORY VESSEL ENLARGEMENT, NOT INTIMAL FORMATION, ACCOUNT FOR RESTENOSIS AFTER ANGIOPLASTY IN THE HYPERCHOLESTEROLEMIC RABBIT MODEL [J].
KAKUTA, T ;
CURRIER, JW ;
HAUDENSCHILD, CC ;
RYAN, TJ ;
FAXON, DP .
CIRCULATION, 1994, 89 (06) :2809-2815
[32]   Dose-dependent limitation of arterial enlargement by the matrix metalloproteinase inhibitor RS-113,456 [J].
Karwowski, JK ;
Markezich, A ;
Whitson, J ;
Abbruzzese, TA ;
Zarins, CK ;
Dalman, RL .
JOURNAL OF SURGICAL RESEARCH, 1999, 87 (01) :122-129
[33]   RESTENOSIS AFTER EXPERIMENTAL ANGIOPLASTY - INTIMAL, MEDIAL, AND ADVENTITIAL CHANGES ASSOCIATED WITH CONSTRICTIVE REMODELING [J].
LAFONT, A ;
GUZMAN, LA ;
WHITLOW, PL ;
GOORMASTIC, M ;
CORNHILL, JF ;
CHISOLM, GM .
CIRCULATION RESEARCH, 1995, 76 (06) :996-1002
[34]   Arterial remodeling: Relation to hemodynamics [J].
Langille, BL .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1996, 74 (07) :834-841
[35]   The peptidase zymogen proregions: Nature's way of preventing undesired activation and proteolysis [J].
Lazure, C .
CURRENT PHARMACEUTICAL DESIGN, 2002, 8 (07) :511-531
[36]   PROPERTIES AND SUBCELLULAR-LOCALIZATION OF ELASTASE-LIKE ACTIVITIES OF ARTERIAL SMOOTH-MUSCLE CELLS IN CULTURE [J].
LEAKE, DS ;
HORNEBECK, W ;
BRECHEMIER, D ;
ROBERT, L ;
PETERS, TJ .
BIOCHIMICA ET BIOPHYSICA ACTA, 1983, 761 (01) :41-47
[37]   Circumferential stress and matrix metalloproteinase 1 in human coronary atherosclerosis - Implications for plaque rupture [J].
Lee, RT ;
Schoen, FJ ;
Loree, HM ;
Lark, MW ;
Libby, P .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 1996, 16 (08) :1070-1073
[38]   Arterial repair after stenting and the effects of GM6001, a matrix metalloproteinase inhibitor [J].
Li, C ;
Cantor, WJ ;
Nili, N ;
Robinson, R ;
Fenkell, L ;
Le Tran, Y ;
Whittingham, HA ;
Tsui, W ;
Cheema, AN ;
Sparkes, JD ;
Pritzker, K ;
Levy, DE ;
Strauss, BH .
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY, 2002, 39 (11) :1852-1858
[39]  
Libby P, 2001, AM J CARDIOL, V88, p3J
[40]  
Lijnen HR, 1999, CIRC RES, V85, P1186