Mechanisms of immunothrombosis in COVID-19.
Journal
Current opinion in hematology
ISSN: 1531-7048
Titre abrégé: Curr Opin Hematol
Pays: United States
ID NLM: 9430802
Informations de publication
Date de publication:
01 11 2021
01 11 2021
Historique:
pubmed:
8
7
2021
medline:
21
10
2021
entrez:
7
7
2021
Statut:
ppublish
Résumé
Coronavirus disease 2019 (COVID-19) is an infectious disease caused by severe acute respiratory syndrome coronavirus-2. Over the past year, COVID-19 has posed a significant threat to global health. Although the infection is associated with mild symptoms in many patients, a significant proportion of patients develop a prothrombotic state due to a combination of alterations in coagulation and immune cell function. The purpose of this review is to discuss the pathophysiological characteristics of COVID-19 that contribute to the immunothrombosis. Endotheliopathy during COVID-19 results in increased multimeric von Willebrand factor release and the potential for increased platelet adhesion to the endothelium. In addition, decreased anticoagulant proteins on the surface of endothelial cells further alters the hemostatic balance. Soluble coagulation markers are also markedly dysregulated, including plasminogen activator inhibitor-1 and tissue factor, leading to COVID-19 induced coagulopathy. Platelet hyperreactivity results in increased platelet-neutrophil and -monocyte aggregates further exacerbating the coagulopathy observed during COVID-19. Finally, the COVID-19-induced cytokine storm primes neutrophils to release neutrophil extracellular traps, which trap platelets and prothrombotic proteins contributing to pulmonary thrombotic complications. Immunothrombosis significantly contributes to the pathophysiology of COVID-19. Understanding the mechanisms behind COVID-19-induced coagulopathy will lead to future therapies for patients.
Identifiants
pubmed: 34232139
doi: 10.1097/MOH.0000000000000666
pii: 00062752-202111000-00012
pmc: PMC8490282
mid: NIHMS1717495
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
445-453Subventions
Organisme : NIA NIH HHS
ID : K01 AG059892
Pays : United States
Organisme : NINDS NIH HHS
ID : U24 NS107228
Pays : United States
Informations de copyright
Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.
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