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Fig. 3 | Cardiovascular Diabetology

Fig. 3

From: Mechanisms of endothelial activation, hypercoagulation and thrombosis in COVID-19: a link with diabetes mellitus

Fig. 3

Hypercoagulability and hypofibrinolysis in COVID-19 and DM. Disrupted hemostasis during COVID-19 may be further intensified under diabetic milieu, resulting in a hypercoagulant phenotype of the activated EC. Elevated levels of pro-coagulant factors (VWF, FVIII, TF/TFPI, thrombin and fibrin) and diminished or insufficient anti-coagulant mediators (ADAMST-13, tPA-plasminogen, KKS, aPC-EPCR) may alter the thrombosis and thrombolysis equilibrium towards formation of blood clots. Arrows indicate over- or down-regulation of factors in COVID-19 (blue) or in DM (green) pathology. Drugs against specific mediators are shown in red beside its target of action. VWF (von Willebrand factor), FVIII (factor VIII), TF (tissue factor), HMWK (high molecular weight kininogen), PK (plasma kallikrein), LMWH (low molecular weight heparin), FXa (activated factor X), aPC (activated protein C), EPCR (endothelial cell protein C receptor), tPA (tissue plasminogen activator), PAI-1 (tissue plasminogen activator), TAFI (thrombin activatable fibrinolysis inhibitor)

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