Mineralocorticoid receptor-antagonism prevents COVID-19-dependent glycocalyx damage

Benedikt Fels*, Sovon Acharya, Carl Vahldieck, Tobias Graf, Nadja Käding, Jan Rupp, Kristina Kusche-Vihrog

*Corresponding author for this work

Abstract

Proinflammatory cytokines target vascular endothelial cells during COVID-19 infections. In particular, the endothelial glycocalyx (eGC), a proteoglycan-rich layer on top of endothelial cells, was identified as a vulnerable, vasoprotective structure during infections. Thus, eGC damage can be seen as a hallmark in the development of endothelial dysfunction and inflammatory processes. Using sera derived from patients suffering from COVID-19, we could demonstrate that the eGC became progressively worse in relation to disease severity (mild vs severe course) and in correlation to IL-6 levels. This could be prevented by administering low doses of spironolactone, a well-known and highly specific aldosterone receptor antagonist. Our results confirm that SARS-CoV-2 infections cause eGC damage and endothelial dysfunction and we outline the underlying mechanisms and suggest potential therapeutic options.

Original languageEnglish
JournalPflugers Archiv European Journal of Physiology
Volume474
Issue number10
Pages (from-to)1069-1076
Number of pages8
ISSN0031-6768
DOIs
Publication statusPublished - 10.2022

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)

DFG Research Classification Scheme

  • 204-05 Immunology

Coronavirus related work

  • Research on SARS-CoV-2 / COVID-19

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