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

Ryan A. Seth, Thomas A. J. McKinnon, Xiao Hui Zhang

2021American Journal of Physiology-Heart and Circulatory Physiology31 citationsDOIOpen Access PDF

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.

Topics & Concepts

ADAMTS13CoagulopathyVon Willebrand factorMedicineImmunologyCoronavirus disease 2019 (COVID-19)DisintegrinEndothelial dysfunctionCoronavirusDiseaseMetalloproteinaseInternal medicinePlateletInfectious disease (medical specialty)Matrix metalloproteinaseCOVID-19 Clinical Research StudiesComplement system in diseasesBlood Coagulation and Thrombosis Mechanisms
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