As such, it is highly significant to better characterize pathophysiological pathways involved in COVID-19-associated vasculopathy and to identify novel therapeutic strategies to curb endothelial dysfunction in both acute SARS-CoV-2 infection and in post-acute sequelae, as can occur in long COVID.
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Direct endothelial ENaC activation mitigates vasculopathy induced by SARS-CoV2 spike protein.
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