Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19
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Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID‑19 Mario Bautista‑Vargas1 · Fabio Bonilla‑Abadía1 · Carlos A. Cañas1
© Springer Science+Business Media, LLC, part of Springer Nature 2020
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 metallocarboxypeptidase, 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 COVID-19 · SARS-CoV-2 · Tissue factor · IL-6 · TNF-α · Thrombosis
Highlights • Severe forms of Covid-19 are related to thrombotic coag-
ulopathy. Its pathogenesis involves the effect of the virus on the immune system and the downregulation of ACE2 that causes an increase in angiotensin II levels. • Tissue factor is likely involved in this chain of events. Both proinflammatory cytokines and increased angiotensin II are known factors in its induction.
Introduction In December 2019, a new and highly contagious infectious disease emerged in the city of Wuhan, China [1]. Some of the infected patients developed severe acute respiratory syndrome (SARS) and a systemic inflammatory response syndrome (SIRS) associated with high mortality [2]. This * Carlos A. Cañas [email protected] 1
Unit of Rheumatology, Fundación Valle del Lili, Universidad Icesi, Avenida Simón Bolívar Cra.98 No.18‑49, Cali, Colombia
disease rapidly disseminated worldwide and was declared to be a pandemic in March 2020 [3]. The causative agent of the new disease, Coronavirus Disease-2019 (COVID-19), was isolated and identified as a novel coronavirus, now known as Severe Acute Respiratory Syndrome Coronavirus-2 (SARSCoV-2). The pathway for virus entry into target cells is analogous to that used by epidemic SARS-CoV and includes a union between the viral surface S protein and its target membrane receptor, angiotensin converting enzyme 2 (ACE-2) that has been identified on cells of the respiratory epithelium [4]. Triggers numerous immunological and inflammatory responses that promote distinct clinical manifestations of COVID-19 [5]. The immune/inflammatory response may be self-limited in patients who experience mild symptoms and who have good p
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