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Am J Physiol Heart Circ Physiol . Contribution of the von Willebrand Factor/ADAMTS13 Imbalance to COVID-19 Coagulopathy

tetano

Editor, Senior Moderator
Am J Physiol Heart Circ Physiol


. 2021 Dec 10.
doi: 10.1152/ajpheart.00204.2021. Online ahead of print.
Contribution of the von Willebrand Factor/ADAMTS13 Imbalance to COVID-19 Coagulopathy


Ryan Seth[SUP] 1 [/SUP], Thomas A J McKinnon[SUP] 2 [/SUP], X Frank Zhang[SUP] 1 [/SUP]



Affiliations

Abstract

The 2019 coronavirus disease (COVID-19) is the disease caused by SARS-CoV-2 infection. While this infection has been shown to affect the respiratory system, a high incidence of thrombotic events has been observed in severe cases of COVID-19 and in a significant portion of COVID-19 non-survivors. While prior literature has reported on both the coagulopathy and hypercoagulability of COVID-19, the specifics of coagulation have not been fully investigated. Observations of microthrombosis in COVID-19 patients have brought attention to potential inflammatory endothelial injury. Von Willebrand factor (VWF) and its protease, a disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13 (ADAMTS13), play an important homeostatic role in responding to endothelial injury. This report provides an overview of the literature investigating the role the VWF/ADAMTS13 axis may have in COVID-19 thrombotic events and suggests potential therapeutic strategies to prevent the progression of coagulopathy in COVID-19 patients.

Keywords: COVID-19; Coagulopathy; Endothelium; Thrombosis; von Willebrand Factor.
 
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