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2020 ; 7
(1
): ä Nephropedia Template TP
gab.com Text
Twit Text FOAVip
Twit Text #
English Wikipedia
Thrombotic complications of COVID-19 may reflect an upregulation of endothelial
tissue factor expression that is contingent on activation of endosomal NADPH
oxidase
#MMPMID32532805
DiNicolantonio JJ
; McCarty M
Open Heart
2020[Jun]; 7
(1
): ä PMID32532805
show ga
The high rate of thrombotic complications associated with COVID-19 seems likely
to reflect viral infection of vascular endothelial cells, which express the ACE2
protein that enables SARS-CoV-2 to invade cells. Various proinflammatory stimuli
can promote thrombosis by inducing luminal endothelial expression of tissue
factor (TF), which interacts with circulating coagulation factor VII to trigger
extrinsic coagulation. The signalling mechanism whereby these stimuli evoke TF
expression entails activation of NADPH oxidase, upstream from activation of the
NF-kappaB transcription factor that drives the induced transcription of the TF
gene. When single-stranded RNA viruses are taken up into cellular endosomes, they
stimulate endosomal formation and activation of NADPH oxidase complexes via
RNA-responsive toll-like receptor 7. It is therefore proposed that SARS-CoV-2
infection of endothelial cells evokes the expression of TF which is contingent on
endosomal NADPH oxidase activation. If this hypothesis is correct,
hydroxychloroquine, spirulina (more specifically, its chromophore
phycocyanobilin) and high-dose glycine may have practical potential for
mitigating the elevated thrombotic risk associated with COVID-19.