Fig. 1
COVID-19 and hemostasis regulation. SARS-CoV-2 may infect endothelial cells (EC) causing endothelitis and directly disrupting endothelial homeostasis, leading to cytokine release, and favoring a pro-coagulant micro-environment. Then, primary hemostasis can be induced by fast vasoconstriction and release of pro-inflammatory and pro-contractile endothelial factors. Activation of coagulation cascades weaves thrombin and fibrin networks that immobilize erythrocytes and activated platelets to from a blood clot in the secondary hemostasis. The resolution of coagulation (tertiary hemostasis) may be also damaged in COVID-19 by alterations in the plasminogen-plasmin and thrombin/thrombomodulin-EPCRP-aPC pathways. Hyperinflammation, hypercoagulation, and hypofibrinolysis could be responsible for thrombotic events in COVID-19 subjects. TXA2 (thromboxane A2), aPC (activated protein C), PC (protein C), EPCR (endothelial protein C receptor)