ArticleCommunications medicine2023
Myeloperoxidase inhibition may protect against endothelial glycocalyx shedding induced by COVID-19 plasma.
Article in Communications medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
What it found
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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
10 citing papers in PubMed, 1 synthesis or guideline pooled it, 15 citations in OpenAlex.
- Salivary Alterations of Myeloperoxidase in Patients with Systemic Diseases: A Systematic Review.International journal of molecular sciences · 2023Pooled it
- Diagnostic and pathophysiological significance of serum myeloperoxidase, ischemia-modified albumin, paraoxonase-1 and galectin-3 in COVID-19 - parallels with myocarditis.BMC cardiovascular disorders · 2026Article
- Digoxin attenuates LPS-induced acute lung injury in mice via NF-κB and HIF-1α inhibition.Biomolecules & biomedicine · 2026Article
- Circulating angiogenic progenitor cell apoptosis in Post-COVID-19 syndrome.International journal of cardiology. Heart & vasculature · 2026Article
- Neutrophil Dynamics in Viral Infections: Drivers of Inflammation and Targets for Pro-Resolving Therapies.Journal of innate immunity · 2026Review
- Chronic Obstructive Pulmonary Disease and COVID-19: The Impact of Hematological Biomarkers on Disease Severity and Outcomes.Journal of clinical medicine · 2025Review
- Association of inflammation and protein carbamylation in patients with COVID-19.Frontiers in medicine · 2025Article
- Myeloperoxidase as a Promising Therapeutic Target after Myocardial Infarction.Antioxidants (Basel, Switzerland) · 2024Review
- Protecting the endothelial glycocalyx in COVID-19.PLoS pathogens · 2024Article
- The Roles of Neutrophil-Derived Myeloperoxidase (MPO) in Diseases: The New Progress.Antioxidants (Basel, Switzerland) · 2024Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundSARS-CoV-2, the causative agent of COVID-19, is a threat to public health. Evidence suggests increased neutrophil activation and endothelial glycocalyx (EG) damage are independently associated with severe COVID-19. Here, we hypothesised that an increased level of blood neutrophil myeloperoxidase (MPO) is associated with soluble EG breakdown, and inhibiting MPO activity may reduce EG damage.
methodsAnalysing a subset of acute and convalescent COVID-19 plasma, 10 from severe and 15 from non-severe COVID-19 cases, and 9 from pre-COVID-19 controls, we determined MPO levels, MPO activity and soluble EG proteins (syndecan-1 and glypican-1) levels by enzyme-linked immunosorbent assay. In vitro primary human aortic endothelial cells were cultured with plasma untreated or treated with specific MPO inhibitors (MPO-IN-28, AZD5904) to determine EG shedding. We then investigated whether inhibiting MPO activity decreased EG degradation.
resultsIn COVID-19 plasma, MPO levels, MPO activity and levels of soluble EG proteins are significantly raised compared to controls, and concentrations increase in proportion to disease severity. Despite clinical recovery, protein concentrations remain significantly elevated. Interestingly, there is a trend of increasing MPO activity in convalescent plasma in both severe and non-severe groups. MPO levels and MPO activity correlate significantly with soluble EG levels and inhibiting MPO activity leads to reduced syndecan-1 shedding, in vitro.
conclusionsNeutrophil MPO may increase EG shedding in COVID-19, and inhibiting MPO activity may protect against EG degradation. Further research is needed to evaluate the utility of MPO inhibitors as potential therapeutics against severe COVID-19.
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.