Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19.
J Thromb Thrombolysis
; 50(3): 479-483, 2020 Oct.
Article
in English
| MEDLINE | ID: covidwho-591509
ABSTRACT
In December 2019, a new and highly contagious infectious disease emerged in Wuhan, China. The etiologic agent was identified as a novel coronavirus, now known as Severe Acute Syndrome Coronavirus-2 (SARS-CoV-2). Recent research has revealed that virus entry takes place upon the union of the virus S surface protein with the type I transmembrane metallo-carboxypeptidase, angiotensin converting enzyme 2 (ACE-2) identified on epithelial cells of the host respiratory tract. Virus triggers the synthesis and release of pro-inflammatory cytokines, including IL-6 and TNF-α and also promotes downregulation of ACE-2, which promotes a concomitant increase in levels of angiotensin II (AT-II). Both TNF-α and AT-II have been implicated in promoting overexpression of tissue factor (TF) in platelets and macrophages. Additionally, the generation of antiphospholipid antibodies associated with COVID-19 may also promote an increase in TF. TF may be a critical mediator associated with the development of thrombotic phenomena in COVID-19, and should be a target for future study.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Pneumonia, Viral
/
Thrombosis
/
Blood Coagulation
/
Thromboplastin
/
Coronavirus Infections
/
Betacoronavirus
Type of study:
Diagnostic study
/
Etiology study
Limits:
Animals
/
Humans
Language:
English
Journal:
J Thromb Thrombolysis
Journal subject:
Vascular Diseases
Year:
2020
Document Type:
Article
Affiliation country:
S11239-020-02172-x
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