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Redox Rep. 2017 Mar;22(2):51-73. doi: 10.1080/13510002.2016.1256119. Epub 2016 Nov 25.

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture.

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a Vascular Biology Division , Victor Chang Cardiac Research Institute , Darlinghurst , New South Wales , Australia.
b Department of Cardiology , Prince of Wales Hospital , Randwick , New South Wales , Australia.
c Faculty of Medicine , University of New South Wales , Sydney , New South Wales , Australia.
d School of Medical Sciences , University of New South Wales , Sydney , New South Wales , Australia.


Atherosclerosis is the main pathophysiological process underlying coronary artery disease (CAD). Acute complications of atherosclerosis, such as myocardial infarction, are caused by the rupture of vulnerable atherosclerotic plaques, which are characterized by thin, highly inflamed, and collagen-poor fibrous caps. Several lines of evidence mechanistically link the heme peroxidase myeloperoxidase (MPO), inflammation as well as acute and chronic manifestations of atherosclerosis. MPO and MPO-derived oxidants have been shown to contribute to the formation of foam cells, endothelial dysfunction and apoptosis, the activation of latent matrix metalloproteinases, and the expression of tissue factor that can promote the development of vulnerable plaque. As such, detection, quantification and imaging of MPO mass and activity have become useful in cardiac risk stratification, both for disease assessment and in the identification of patients at risk of plaque rupture. This review summarizes the current knowledge about the role of MPO in CAD with a focus on its possible roles in plaque rupture and recent advances to quantify and image MPO in plasma and atherosclerotic plaques.


Atherosclerosis; cardiovascular disease; coronary artery disease; imaging; myeloperoxidase; plaque rupture; reactive oxygen species; vulnerable plaques

[Indexed for MEDLINE]

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