Myeloperoxidase (MPO), a heme protein abundantly expressed by neutrophils, monocytes and macrophages, has been suggested to critically accelerate the course of vascular inflammatory disease: Myeloperoxidase not only has been localized to atherosclerotic plaques, it also binds to and transcytopses endothelial cells to accumulate in the subendothelial space. Here, MPO remains catalytically active and is capable of oxidizing lipoproteins, matrix proteins and nitric oxide, thereby adversely affecting endothelial function.
Multiple clinical trials suggest that circulating MPO levels identify patients with stable and unstable coronary artery disease as well as those with heart failure and peripheral vascular disease, who are at risk for adverse cardiovascular events. Given the powerful proinflammatory properties of this enzyme, MPO suggests to be both marker and mediator of cardiovascular pathology and emerges as both marker and potential target of treatment.
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