Fig. 2
The EC activation and dysfunction, as a central pathophysiological mechanism of COVID-19 coagulopathy. SARS-CoV-2 infection and its concomitant local and systemic immunogenic stimuli (cytokine storm, vasoactive compounds, NETosis, and activated complement system) disrupt endothelial homeostasis leading to EC activation. This activation comprises over-inflammation, loss of endothelial barrier integrity and altered hemostasis, favoring coagulation and thrombosis. In red, specific drugs against mediators of endothelial activation. ARDS (acute respiratory distress syndrome), IL (interleukin), TNF-α (tumor necrosis factor alpha), Ang-(1-7) (angiotensin-(1-7)), NO (nitric oxide), Ang II (angiotensin II), TXA2 (thromboxane A2), MAC (membrane attack complex), TLR-4 (toll-like receptor 4)