COVID-19: a probable role of the anticoagulant Protein S in managing COVID-19-associated coagulopathy

The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called "cytokine storm" and coagulopathy. Hypoxia is also as...

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Bibliographic Details
Published in:Aging (Albany, NY.) NY.), 2020-08, Vol.12 (16), p.15954-15961
Main Authors: Chatterjee, Sabyasachi, Sengupta, Tanusree, Majumder, Samarpan, Majumder, Rinku
Format: Article
Language:English
Subjects:
Angiotensin-Converting Enzyme 2
Anticoagulants - metabolism
Anticoagulants - pharmacology
Betacoronavirus - physiology
Coronavirus Infections - blood
Coronavirus Infections - immunology
Coronavirus Infections - therapy
COVID-19
Cytokine Release Syndrome - blood
Cytokine Release Syndrome - virology
Disease Management
Humans
Hypoxia - blood
Hypoxia - etiology
Hypoxia - immunology
Interleukin-6 - blood
Pandemics
Peptidyl-Dipeptidase A - metabolism
Pneumonia, Viral - blood
Pneumonia, Viral - immunology
Pneumonia, Viral - therapy
Protein S - metabolism
Protein S - pharmacology
Research Paper
SARS-CoV-2
Severity of Illness Index
Thrombophilia - immunology
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Summary:The COVID-19 pandemic has caused monumental mortality, and there are still no adequate therapies. Most severely ill COVID-19 patients manifest a hyperactivated immune response, instigated by interleukin 6 (IL6) that triggers a so called "cytokine storm" and coagulopathy. Hypoxia is also associated with COVID-19. So far overlooked is the fact that both IL6 and hypoxia depress the abundance of a key anticoagulant, Protein S. We speculate that the IL6-driven cytokine explosion plus hypoxemia causes a severe drop in Protein S level that exacerbates the thrombotic risk in COVID-19 patients. Here we highlight a mechanism by which the IL6-hypoxia curse causes a deadly hypercoagulable state in COVID-19 patients, and we suggest a path to therapy.
ISSN:1945-4589
1945-4589
DOI:10.18632/aging.103869