Evidence map›Paper›PMID 39061857›Full record

ReviewAntioxidants (Basel, Switzerland)2024

Myeloperoxidase as a Promising Therapeutic Target after Myocardial Infarction.

Maxwell Quinn, Richard Y K Zhang, Idris Bello, Kerry-Anne Rye, Shane R Thomas

Abstract readReview
In one paragraph

Review in Antioxidants (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  6. Article
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  9. Review
  10. Article
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  13. Exploring Neutrophil Extracellular Traps in Cardiovascular Pathologies: The Impact of Lipid Profiles, PAD4, and Radiation.Biocell : official journal of the Sociedades Latinoamericanas de Microscopia Electronica ... et. al · 2025
    Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Maxwell QuinnCardiometabolic Disease Research Group, School of Biomedical Sciences, Faculty of Medicine & Health, University of New South Wales, Sydney, NSW 2052, Australia.
Richard Y K ZhangCardiometabolic Disease Research Group, School of Biomedical Sciences, Faculty of Medicine & Health, University of New South Wales, Sydney, NSW 2052, Australia.ORCID 0000-0003-4432-8545
Idris BelloCardiometabolic Disease Research Group, School of Biomedical Sciences, Faculty of Medicine & Health, University of New South Wales, Sydney, NSW 2052, Australia.
Kerry-Anne RyeCardiometabolic Disease Research Group, School of Biomedical Sciences, Faculty of Medicine & Health, University of New South Wales, Sydney, NSW 2052, Australia.ORCID 0000-0002-9751-917X
Shane R ThomasCardiometabolic Disease Research Group, School of Biomedical Sciences, Faculty of Medicine & Health, University of New South Wales, Sydney, NSW 2052, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary artery disease (CAD) and myocardial infarction (MI) remain leading causes of death and disability worldwide. CAD begins with the formation of atherosclerotic plaques within the intimal layer of the coronary arteries, a process driven by persistent arterial inflammation and oxidation. Myeloperoxidase (MPO), a mammalian haem peroxidase enzyme primarily expressed within neutrophils and monocytes, has been increasingly recognised as a key pro-inflammatory and oxidative enzyme promoting the development of vulnerable coronary atherosclerotic plaques that are prone to rupture, and can precipitate a MI. Mounting evidence also implicates a pathogenic role for MPO in the inflammatory process that follows a MI, which is characterised by the rapid infiltration of activated neutrophils into the damaged myocardium and the release of MPO. Excessive and persistent cardiac inflammation impairs normal cardiac healing post-MI, resulting in adverse cardiac outcomes and poorer long-term cardiac function, and eventually heart failure. This review summarises the evidence for MPO as a significant oxidative enzyme contributing to the inappropriate inflammatory responses driving the progression of CAD and poor cardiac healing after a MI. It also details the proposed mechanisms underlying MPO's pathogenic actions and explores MPO as a novel therapeutic target for the treatment of unstable CAD and cardiac damage post-MI.

Indexed as

atherosclerosisheart failureleft ventricular remodellingmyeloperoxidasemyocardial infarctionoxidative stress

Identifiers

PMID39061857
PMCPMC11274265

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.