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


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
Issue number10
Pages (from-to)1069-1076
Number of pages8
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


Dive into the research topics of 'Mineralocorticoid receptor-antagonism prevents COVID-19-dependent glycocalyx damage'. Together they form a unique fingerprint.

Cite this