Coagulation abnormalities in SARS-CoV-2 infection: overexpression tissue factor

Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the increased risk of some life-threatening compli...

Full description

Saved in:
Bibliographic Details
Published in:Thrombosis journal 2020-12, Vol.18 (1), p.38-38, Article 38
Main Authors: Eslamifar, Zahra, Behzadifard, Mahin, Soleimani, Masoud, Behzadifard, Saba
Format: Article
Language:English
Subjects:
Angiotensin converting enzyme
Coagulopathy
Coronaviruses
COVID-19
Heart attack
Infection
Ischemia
Lymphocytes
Macrophages
Mortality
Pulmonary embolism
Review
SARS-CoV-2
Severe acute respiratory syndrome coronavirus 2
Stroke (Disease)
Thrombosis
Tissue factor
Tumor necrosis factor
Viral infections
Virus diseases
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Among the pathways and mediators that may be dysregulated in COVID-19 infection, there are proinflammatory cytokines, lymphocyte apoptosis, and the coagulation cascade. Venous and arterial thromboembolisms also are frequent in COVID-19 patients with the increased risk of some life-threatening complications such as pulmonary embolism, myocardial infarction, and ischemic stroke. In this regard, overproduction of proinflammatory cytokines such as IL-6, IL-1β, and TNF-α induce cytokine storms, increase the risk of clot formation, platelet activation, and multiorgan failure that may eventually lead to death among these patients. Surface S protein of SARS-CoV-2 binds to its target transmembrane receptor, named as angiotensin converting enzyme 2 (ACE2(, on various cells such as lymphocyte, alveolar cells, monocytes/macrophages, and platelets. Notably, the activation of the coagulation cascade occurs through tissue factor (TF)/FVIIa-initiated hemostasis. Accordingly, TF plays the major role in the activation of coagulation system during viral infection. In viral infections, the related coagulopathy multiple factors such as inflammatory cytokines and viral specific TLRs are involved, which consequently induce TF expression aberrantly. SARS-COV-2 may directly infect monocytes/ macrophages. In addition, TF expression/release from these cells may play a critical role in the development of COVID-19 coagulopathy. In this regard, the use of TF- VIIa complex inhibitor may reduce the cytokine storm and mortality among COVID-19 patients.
ISSN:1477-9560
1477-9560
DOI:10.1186/s12959-020-00250-x