Open AccessContribution of the von Willebrand factor/ADAMTS13 imbalance to COVID-19 coagulopathy
Author(s) -
Ryan A. Seth,
Thomas A. J. McKin,
Xiao Hui Zhang
Publication year - 2022
Publication title -
american journal of physiology. heart and circulatory physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.524
H-Index - 197
eISSN - 1522-1539
pISSN - 0363-6135
DOI - 10.1152/ajpheart.00204.2021
Subject(s) - adamts13 , coagulopathy , von willebrand factor , medicine , immunology , covid-19 , disintegrin , endothelial dysfunction , coronavirus , disease , metalloproteinase , platelet , infectious disease (medical specialty) , matrix metalloproteinase
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.