ReviewRedox report : communications in free radical research2017
The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture.
Review in Redox report : communications in free radical research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 188 citations in OpenAlex.
- Salivary Alterations of Myeloperoxidase in Patients with Systemic Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- The myeloperoxidase inhibitor mitiperstat (AZD4831) does not prolong the QT interval at expected therapeutic doses.Pharmacology research & perspectives · 2024Trial
- Review
- The Wound-Heart Axis: Can Chronic Wounds Contribute to Cardiac Dysfunction?International journal of molecular sciences · 2026Review
- Relationship between the oxidative stress biomarkers and coronary heart disease: Pathogenesis to therapeutic aspects.World journal of cardiology · 2026Review
- Myeloperoxidase as a therapeutic target for oxidative damage in Alzheimer's disease.Journal of enzyme inhibition and medicinal chemistry · 2025Review
- An Optimized Protocol for Enzymatic Hypothiocyanous Acid Synthesis.Methods and protocols · 2025Article
- Isoform-specific oxidative modifications of tropoelastin by HOCl and MPO alter protein self-assembly.Redox report : communications in free radical research · 2025Article
- Inflammatory microenvironment-responsive MR imaging contrast agents.Nanomedicine (London, England) · 2025Review
- Review
- "The NET effect": Neutrophil extracellular traps-a potential key component of the dysregulated host immune response in sepsis.Critical care (London, England) · 2025Review
- Protein carbamylation in atherosclerotic plaques correlates with uremia and disease progression, localizing predominantly to foam cells.Frontiers in immunology · 2025Article
- Environment-sensitive turn-on fluorescent probe enables live cell imaging of myeloperoxidase activity during NETosis.Communications chemistry · 2024Article
- The Role of Inducible Nitric Oxide Synthase in Assessing the Functional Level of Coronary Artery Lesions in Chronic Coronary Syndrome.Cardiology research · 2024Review
- Childhood Cardiovascular Health, Obesity, and Some Related Disorders: Insights into Chronic Inflammation and Oxidative Stress.International journal of molecular sciences · 2024Review
- Review
- TheInnate immunity · 2024Article
- Propolis Reduces Inflammation and Dyslipidemia Caused by High-Cholesterol Diet in Mice by Lowering ADAM10/17 Activities.Nutrients · 2024Article
- Photodynamic Therapy for Atherosclerosis.International journal of molecular sciences · 2024Review
- The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress.Antioxidants (Basel, Switzerland) · 2024Review
28 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
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.