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Review
. 2022 Jan 1;322(1):H87-H93.
doi: 10.1152/ajpheart.00204.2021. Epub 2021 Dec 10.

Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy

Affiliations
Review

Contribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy

Ryan Seth et al. Am J Physiol Heart Circ Physiol. .

Abstract

The 2019 coronavirus disease (COVID-19) is the disease caused by SARS-CoV-2 infection. Although 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 nonsurvivors. Although 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 patients with COVID-19 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 patients with COVID-19.

Keywords: COVID-19; coagulopathy; endothelium; thrombosis; von Willebrand factor.

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Conflict of interest statement

No conflicts of interest, financial or otherwise, are declared by the authors.

Figures

Figure 1.
Figure 1.
A: schematic illustration of VWF’s domain arrangement and the key functions of the A domains. B: model connecting viral infection, endothelial injury, the VWF/ADAMTS13 axis, and COVID-19 coagulopathy. Created with BioRender.com and published with permission. ADAMTS13, A disintegrin and metalloproteinase with a thrombospondin type 1 motif, member 13; VWF, von Willebrand factor.

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