Increased Plasma Concentration of Matrix Metalloproteinase-7 in Patients with Coronary Artery Disease (Lipids, Lipoproteins, And Cardiovascular Risk Factors‪)‬

Matrix metalloproteinases (MMPs) (4) constitute a family of closely related proteinases that together have the capacity to degrade all components of the extracellular matrix (ECM) (1, 2). MMPs play important roles during physiologic processes such as embryonic development, wound healing, and angiogenesis, but they have also been implicated in several pathologic conditions, such as atherogenesis and precipitation of acute coronary syndromes (ACS) (3). Plaque rupture is often associated with the breakdown of ECM in the shoulder region of a plaque (4,5). This is supported by the observation that vulnerable plaques, relative to stable plaques, contain low amounts of ECM (6, 7). ECM breakdown is mediated by proteinases, in particular MMPs, which are being overexpressed in the shoulder region of atherosclerotic plaques (3). Coronary artery disease (CAD) is characterized by focal inflammation of the arterial wall. MMPs and tissue inhibitors of MMPs (TIMPs) are secreted by different cell types of the vessel wall (8-11). The inflammation process modulates the secretion of various MMPs and TIMPs from these cells (3), thereby promoting atherogenesis, plaque rupture, and thrombosis. In conditions of arterial inflammation, such as temporal arteritis, serum or plasma concentrations of MMPs are generally altered (12, 13). It is therefore reasonable to assume that the plasma or serum concentrations of MMPs may reflect MMP activity within the vessel wall.