id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-263457-puf8gjir	Jayarangaiah, Apoorva	COVID-19-Associated Coagulopathy: An Exacerbated Immunothrombosis Response	2020-07-31		.txt	text/plain	5552	374	34	Activated leukocytes potentiate a procoagulant state via release of intravascular tissue factor, platelet activation, NETosis, and inhibition of anticoagulant mechanisms. 4, 5 The predominant underlying mechanism in COVID-19-related mortality is hypothesized to be widespread tissue damage and endothelial injury from an overactivated immune system via exaggerated T-cell responses and increased cytokine secretion, leading to a cytokine storm. 70 In conclusion, a viral-mediated coagulant state culminates in the presence of endothelial injury and dysfunction and cytokine-driven inflammatory conditions, leading to activation of TF-mediated thrombosis. The current COVID-19 pandemic has resurrected the concept of immunothrombosis as it is a relevant model to demonstrate the potentiating effects of the immune system and the coagulation system and the detrimental effects associated with their unrestrained activation, as evidenced by microthrombi and overt venous and arterial thrombi (Figure 4 ). A procoagulant state in COVID-19 is the result of a direct viral-related endothelial injury, leukocyte-and cytokinemediated platelet activation, TF release, and NETosis augmented by an unchecked activation of the complement system.	./cache/cord-263457-puf8gjir.txt	./txt/cord-263457-puf8gjir.txt