The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture
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Updated: Mar 11, 2026

Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
Nathaniel Teng1,2, Ghassan J Maghzal1, Jihan Talib1
1a Vascular Biology Division , Victor Chang Cardiac Research Institute , Darlinghurst , New South Wales , Australia.
Insights
Myeloperoxidase (MPO) plays a key role in atherosclerosis and plaque rupture in coronary artery disease (CAD). Detecting MPO aids in assessing cardiac risk and identifying patients prone to plaque rupture.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Inflammation Biology
Background:
- Atherosclerosis is the primary cause of coronary artery disease (CAD).
- Vulnerable atherosclerotic plaques, prone to rupture, are characterized by inflammation and thin fibrous caps.
- Myeloperoxidase (MPO) is mechanistically linked to inflammation and atherosclerosis development.
Purpose of the Study:
- To review the role of MPO in CAD.
- To highlight MPO's contribution to vulnerable plaque formation and rupture.
- To discuss recent advancements in MPO detection and imaging for risk stratification.
Main Methods:
- Literature review of studies investigating MPO's role in atherosclerosis.
- Analysis of evidence linking MPO to plaque vulnerability markers.
- Summary of techniques for quantifying and imaging MPO in clinical settings.
Main Results:
- MPO contributes to foam cell formation, endothelial dysfunction, and matrix metalloproteinase activation.
- MPO promotes tissue factor expression, a key factor in plaque vulnerability.
- MPO detection and imaging are valuable tools for cardiac risk stratification and identifying rupture-prone plaques.
Conclusions:
- MPO is a critical mediator in the pathogenesis of atherosclerosis and plaque rupture.
- Quantification and imaging of MPO offer promising strategies for improving cardiac risk assessment in CAD patients.
- Targeting MPO may represent a future therapeutic approach for managing CAD complications.
Abstract:
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.
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