Abstract
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endopeptidases responsible for tissue remodeling and degradation of extracellular matrix (ECM) proteins. MMPs may modulate various cellular and signaling pathways in atherosclerosis responsible for progression and rupture of atherosclerotic plaques. The effect of MMPs polymorphisms and the expression of MMPs in both the atherosclerotic plaque and plasma was shown. They are independent predictors of atherosclerotic plaque instability in stable coronary heart disease (CHD) patients. Increased levels of MMPs in patients with advanced cardiovascular disease (CAD) and acute coronary syndrome (ACS) was associated with future risk of cardiovascular events. These data confirm that MMPs may be biomarkers in plaque instability as they target in potential drug therapies for atherosclerosis. They provide important prognostic information, independent of traditional risk factors, and may turn out to be useful in improving risk stratification.
Highlights
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endoproteases responsible for tissue remodeling and degradation of extracellular matrix (ECM) proteins [1]
Serum elevation of MMP-2, ADAMTS-1, and ADAMTS-7 is correlated with the initial stages of chronic venous disease (CVD), whereas the serum elevation of MMP-1, MMP-8, MMP-9, NGAL, ADAM-10, ADAM-17, and ADAMTS-4 is involved in skin change complications [9]
Among tissue inhibitors of MMPs (TIMPs), such as tetracyclines, chemically-synthesized small-molecular weight MMP inhibitors and inhibitory antibodies, only doxycycline, which was approved by Food and Drug Administration (FDA), has been evaluated extensively in patients [48]
Summary
Matrix metalloproteinases (MMPs) are a family of zinc-dependent endoproteases responsible for tissue remodeling and degradation of extracellular matrix (ECM) proteins [1]. MMPs family contain 28 members, 23 are expressed in human tissues and 14 are expressed in veins and arteries. They are classified on the basis of their substrates and the organization of their structural domains [3]. MMPs may be inhibited by tissue and biological and synthetic inhibitors [4]. MMPs play important role in maintaining vein wall structure and function, but on the other hand, in adverse cardiovascular remodeling, atherosclerotic plaque formation and plaque instability [7,8]. Collagens I, II, III; fibronectin, laminin-1, dermatan sulfate Large tenascin-C, fibronectin, laminin, entactin, aggrecan, perlecan Collagen III, gelatin, casein, fibronectin Activates MMP2 by cleavage Activates MMP2 by cleavage Inactivates alpha-1 proteinase inhibitor. VSMCs, fibroblasts, macrophages, great saphenous vein Liver Tooth enamel Fibroblasts, macrophages, placenta Ovary, testis Skin, keratinocytes
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