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

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.

Automated summary

Proinflammatory cytokines target the endothelial glycocalyx (eGC) in vascular endothelial cells during COVID-19 infections, leading to endothelial dysfunction. Low doses of spironolactone can prevent the worsening of eGC, suggesting potential therapeutic options.