Endothelin-1 is Increased in the Plasma of Patients Hospitalized with Covid-19

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Authors
Abraham, George
Kuc, Rhoda
Althage, Magnus
Greasley, Peter
Ambery, Philip
  Maguire, Janet
  Wilkinson, Ian
Publication Date
2022-06
Journal Title
Journal of Molecular and Cellular Cardiology
ISSN
0022-2828
Publisher
Elsevier
Type
Article
This Version
VoR
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Citation
Abraham, G., Kuc, R., Althage, M., Greasley, P., Ambery, P., Maguire, J., Wilkinson, I., et al. (2022). Endothelin-1 is Increased in the Plasma of Patients Hospitalized with Covid-19. Journal of Molecular and Cellular Cardiology https://doi.org/10.1016/j.yjmcc.2022.03.007
Abstract
Virus induced endothelial dysregulation is a well-recognised feature of severe Covid-19 infection. Endothelin-1 (ET-1) is the most highly expressed peptide in endothelial cells and a potent vasoconstrictor, thus representing a potential therapeutic target. ET-1 plasma levels were measured in a cohort of 194 Covid-19 patients stratified according to the clinical severity of their illness. Hospitalised patients, including those who died and those developing acute myocardial or kidney injury, had significantly elevated ET-1 plasma levels during the acute phase of infection. The results support the hypothesis that endothelin receptor antagonists may provide clinical benefit for certain Covid-19 patients.
Sponsorship
Supported in full or part by The Jon Moulton Charity Trust, National Institute of Health Research, Cambridge Biomedical Research Centre, BRC-1215-20014 (JC); Wellcome Trust (WT107715/Z/15/Z), Biomedical Resources Grant, University of Cambridge, Cardiovascular Theme RG64226, British Heart Foundation, TG/18/4/33770,
Funder references
Wellcome Trust (107715/Z/15/Z)
British Heart Foundation (TG/18/4/33770)
MRC (via University of Glasgow) (303684)
National Institute for Health Research (IS-BRC-1215-20014)
Identifiers
External DOI: https://doi.org/10.1016/j.yjmcc.2022.03.007
This record's URL: https://www.repository.cam.ac.uk/handle/1810/335274
Rights
Attribution 4.0 International
Licence URL: https://creativecommons.org/licenses/by/4.0/
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Attribution 4.0 International
Except where otherwise noted, this item's licence is described as Attribution 4.0 International