Is myeloperoxidase a biomarker of oxidative stress and vascular inflammation?

Myeloperoxidase (MPO) is an established biomarker that serves as both a primary mediator and a quantitative indicator of oxidative stress and vascular inflammation. Primarily released by activated neutrophils and macrophages, MPO plays a critical role in identifying individuals at risk for cardiovascular pathology.

Clinical and effectiveness evidence

In clinical settings, MPO is a robust predictor of cardiovascular risk, particularly in acute scenarios.

• Cardiovascular Events: Elevated MPO levels are significantly associated with major adverse cardiovascular events (MACE) and mortality, especially in patients presenting with acute coronary syndrome (ACS).
• Vascular Inflammation: High MPO concentrations correlate with markers of systemic inflammation, such as C-reactive protein (CRP), and anatomical indicators like increased carotid intima-media thickness (CIMT).
• Plaque Instability: Research consistently links MPO to endothelial dysfunction and the instability of atherosclerotic plaques, making it a critical tool for assessing vascular health in aging populations.

Mechanistic explanations

MPO drives oxidative burden through its unique enzymatic activity, which generates highly reactive chemical species.

• Halogenative Stress: MPO catalyzes the reaction between hydrogen peroxide and chloride to produce hypochlorous acid (HOCl). This is a primary pathway for "halogenative stress," which causes direct damage to DNA, proteins, and lipids.
• Lipid and Protein Oxidation: Elevated MPO activity is directly correlated with increased malondialdehyde (MDA), a key marker of lipid peroxidation, and higher levels of protein carbonylation.
• LDL Modification: MPO facilitates the oxidation of low-density lipoprotein (LDL) into oxLDL, a process that triggers foam cell formation and the progression of atherosclerosis within the arterial wall.

Bottom line

Myeloperoxidase is a validated biomarker where higher levels directly reflect increased oxidative burden and active vascular inflammation. Its measurement provides critical insight into leukocyte-driven oxidative damage and the stability of the vascular environment, particularly relevant for cardiovascular risk assessment.