Kawasaki-like diseases and thrombotic coagulopathy in COVID-19: delayed over-activation of the STING pathway?
Review
[키워드] ACE2
activate
Activation
aneurysms
Aspirin
binding
bleeding
cell membrane
children
Coagulopathy
Combination
contribute
COVID-19
COVID-19 patient
cytosolic
disease
disorder
DNA
down-regulated
downstream
drug
Herpes virus
Hypothesis
IL-6R
immunoglobulins
Inflammasome
inhibit
inhibited
inhibitor
innate cell
intravenous
IVIG
JAK/STAT pathways
Kawasaki disease
lung tissue
males
mice
monocyte-macrophages
NLRP3
occur
over-expressed
pathway
procoagulant activity
promote
prothrombotic
pyroptosis
reduce
reported
risk
SARS-CoV2
severe COVID-19 patient
severe COVID-19 patients
Signaling
STING
thrombosis
thrombotic
tissue
Tissue Factor
Treatment
triggering
upstream
Vasculitis
viruses
[DOI] 10.1080/22221751.2020.1785336 PMC 바로가기 [Article Type] Review
[DOI] 10.1080/22221751.2020.1785336 PMC 바로가기 [Article Type] Review