ArticlePloS one2019
Myeloperoxidase inhibition in mice alters atherosclerotic lesion composition.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- Oxidative Stress in Cardiovascular Diseases: Mechanisms and Exploring Advanced Therapies.Cardiovascular & hematological agents in medicinal chemistry · 2025Review
- The Role of Antioxidants in the Therapy of Cardiovascular Diseases-A Literature Review.Nutrients · 2024Review
- Myeloperoxidase as a Promising Therapeutic Target after Myocardial Infarction.Antioxidants (Basel, Switzerland) · 2024Review
- The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress.Antioxidants (Basel, Switzerland) · 2024Review
- A potential therapeutic target: The role of neutrophils in the central nervous system.Brain, behavior, & immunity - health · 2023Review
- Combination of Taurine and Black Pepper Extract as a Treatment for Cardiovascular and Coronary Artery Diseases.Nutrients · 2023Review
- Myeloperoxidase PET Imaging Tracks Intracellular and Extracellular Treatment Changes in Experimental Myocardial Infarction.International journal of molecular sciences · 2023Article
- Association of Circulating Neutrophils with Relative Volume of Lipid-Rich Necrotic Core of Coronary Plaques in Stable Patients: A Substudy of SMARTool European Project.Life (Basel, Switzerland) · 2023Article
- Oxidative Stress and Inflammatory Biomarkers for Populations with Occupational Exposure to Nanomaterials: A Systematic Review and Meta-Analysis.Antioxidants (Basel, Switzerland) · 2022Review
- Non-Canonical Functions of Myeloperoxidase in Immune Regulation, Tissue Inflammation and Cancer.International journal of molecular sciences · 2022Review
- Differential dysregulation of granule subsets in WASH-deficient neutrophil leukocytes resulting in inflammation.Nature communications · 2022Article
- Hypochlorous Acid Chemistry in Mammalian Cells-Influence on Infection and Role in Various Pathologies.International journal of molecular sciences · 2022Review
- Cardiovascular disease and ANCA-associated vasculitis: are we missing a beat?Clinical kidney journal · 2022Article
- NETosis as a Pathogenic Factor for Heart Failure.Oxidative medicine and cellular longevity · 2021Review
- Oxidative Stress and Antioxidant Treatments in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2020Review
- Neutrophil-Mediated Cardiac Damage After Acute Myocardial Infarction: Significance of Defining a New Target Cell Type for Developing Cardioprotective Drugs.Antioxidants & redox signaling · 2020Article
- The Role of Thiocyanate in Modulating Myeloperoxidase Activity during Disease.International journal of molecular sciences · 2020Review
- Myeloperoxidase: a potential therapeutic target for coronary artery disease.Expert opinion on therapeutic targets · 2020Review
- Therapeutic targeting of neutrophil exocytosis.Journal of leukocyte biology · 2020Review
- Discontinued Drugs for the Treatment of Cardiovascular Disease from 2016 to 2018.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloperoxidase (MPO) is a highly abundant protein within the neutrophil that is associated with lipoprotein oxidation, and increased plasma MPO levels are correlated with poor prognosis after myocardial infarct. Thus, MPO inhibitors have been developed for the treatment of heart failure and acute coronary syndrome in humans. 2-(6-(5-Chloro-2-methoxyphenyl)-4-oxo-2-thioxo-3,4-dihydropyrimidin-1(2H)-yl)acetamide PF-06282999 is a recently described selective small molecule mechanism-based inactivator of MPO. Here, utilizing PF-06282999, we investigated the role of MPO to regulate atherosclerotic lesion formation and composition in the Ldlr-/- mouse model of atherosclerosis. Though MPO inhibition did not affect lesion area in Ldlr-/- mice fed a Western diet, reduced necrotic core area was observed in aortic root sections after MPO inhibitor treatment. MPO inhibition did not alter macrophage content in and leukocyte homing to atherosclerotic plaques. To assess non-invasive monitoring of plaque inflammation, [18F]-Fluoro-deoxy-glucose (FDG) was administered to Ldlr-/- mice with established atherosclerosis that had been treated with clinically relevant doses of PF-06282999, and reduced FDG signal was observed in animals treated with a dose of PF-06282999 that corresponded with reduced necrotic core area. These data suggest that MPO inhibition does not alter atherosclerotic plaque area or leukocyte homing, but rather alters the inflammatory tone of atherosclerotic lesions; thus, MPO inhibition could have utility to promote atherosclerotic lesion stabilization and prevent atherosclerotic plaque rupture.
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Registered trials
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.