Role of myeloperoxidase in inflammation and atherosclerosis (Review).
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanistic pathways and previously published literature with no new data
PubMed 35620311 · doi:10.3892/br.2022.1536
What was done
This is a narrative review summarizing the physiological and pathological roles of myeloperoxidase (MPO), an enzyme secreted by neutrophils and macrophages, in inflammation and atherosclerosis. The review examines literature on MPO-mediated hypochlorous acid (HOCl) production, low-density lipoprotein (LDL) oxidation, and the utility of MPO as a cardiovascular disease biomarker.
What was found
The abstract reports no numerical data, effect sizes, or diagnostic metrics. It qualitatively describes how MPO generates HOCl at physiological chloride concentrations to produce HOCl-LDL epitopes within atheromatous lesions. This MPO-modified LDL binds scavenger receptors rather than native LDL receptors, promoting endothelial dysfunction and macrophage foam cell formation. The review also notes that elevated MPO levels associate with increased coronary artery disease risk.
Why it matters
It outlines mechanistic pathways connecting innate immune activation and lipid oxidation in atherogenesis, framing MPO as both a cardiovascular risk biomarker and a potential therapeutic target.
Limits
As a narrative review, it lacks a systematic search protocol, study selection criteria, quality appraisal, and meta-analytic pooling. No original human clinical trial or cohort data are presented in the abstract.
Cited by
- supports Neutrophils release the enzyme myeloperoxidase (MPO), which produces hypochlorite (bleach) outside the cell, as well as proteases.