COVID-19 CLOT: What is it? Why in the lungs?Extracellular histone, “auto-activation” of prothrombin, emperipolesis, megakaryocytes, “self-association” of Von Willebrand factor and beyond

COVID-19 thromboembolic disease has brought all of us back to the drawing
board. In COVID-19, pre-existing activated endothelium with increased Von
Willebrand factor (VWF), low density lipoprotein (LDL) promoting “self-association” and “sticking” of long VWF strings to the vascular endothelial wall, suppressed ADAMTS13 cleavage of VWF, hypoxia induced upregulation and activation of VWF, fibrous network from neutrophil extracellular traps (NETs) with free DNA and histone, all appear to be initiating the thrombogenesis. Worsening complement activation, cytokine storm and resulting endothelial destruction, unregulated thrombogenesis leads to vascular occlusions and hypoxia.

COVID-19 CLOT: What is it? Why in the lungs? Extracellular histone, “auto-activation” of prothrombin, emperipolesis, megakaryocytes, “self-association” of Von Willebrand factor and beyond
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