Myeloperoxidase and Atherosclerosis

Abstract

Myeloperoxidase (MPO), a member of the peroxidase family, emerged as a major player in the initiation and propagation of atherosclerotic cardiovascular disease (CVD). Evidence for its role in atherosclerosis include that MPO: a) induces endothelial dysfunction, b) modifies physiologically functional high density lipoprotein (HDL) into “dysfunctional HDL”, c) converts low density lipoprotein (LDL) into more atherogenic modified LDL form, and d) induces endothelial cell death and tissue factor expression involved in plaque vulnerability. Elevated levels of blood MPO are associated with CVD, predict incident risks for myocardial infarction and cardiac death in subjects with acute coronary syndrome, and predict future risk of coronary artery disease (CAD) in healthy individuals. In this article, we review current understandings on the role of MPO in pathophysiological processes involved in atherosclerosis and CVD.