Evidence map›Paper›PMID 33784877›Full record

ReviewClinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis

Role of Tissue Factor in the Pathogenesis of COVID-19 and the Possible Ways to Inhibit It.

Carlos A Cañas, Felipe Cañas, Mario Bautista-Vargas, Fabio Bonilla-Abadía

Open access · goldAbstract readReview
In one paragraph

Review in Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 10% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

21 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.

  1. Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023
    Pooled it
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  8. Article
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  17. COVID-19 Induced Coagulopathy (CIC): Thrombotic Manifestations of Viral Infection.TH open : companion journal to thrombosis and haemostasis · 2022
    Article
  18. Post-COVID syndrome: pulmonary complicationsTurkish journal of medical sciences · 2021
    Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Carlos A CañasUnit of Rheumatology, 67597Fundación Valle del Lili, Universidad Icesi, Cali, Colombia.ORCID https://orcid.org/0000-0002-6879-3700
Felipe CañasUnit of Cardiology, 365750Clínica Medellín, Medellín, Colombia.
Mario Bautista-VargasUnit of Rheumatology, 67597Fundación Valle del Lili, Universidad Icesi, Cali, Colombia.
Fabio Bonilla-AbadíaUnit of Rheumatology, 67597Fundación Valle del Lili, Universidad Icesi, Cali, Colombia.
Fundación Valle del Lili · CO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COVID-19 (Coronavirus Disease 2019) is a highly contagious infection and associated with high mortality rates, primarily in elderly; patients with heart failure; high blood pressure; diabetes mellitus; and those who are smokers. These conditions are associated to increase in the level of the pulmonary epithelium expression of angiotensin-converting enzyme 2 (ACE-2), which is a recognized receptor of the S protein of the causative agent SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2). Severe cases are manifested by parenchymal lung involvement with a significant inflammatory response and the development of microvascular thrombosis. Several factors have been involved in developing this prothrombotic state, including the inflammatory reaction itself with the participation of proinflammatory cytokines, endothelial dysfunction/endotheliitis, the presence of antiphospholipid antibodies, and possibly the tissue factor (TF) overexpression. ARS-Cov-19 ACE-2 down-regulation has been associated with an increase in angiotensin 2 (AT2). The action of proinflammatory cytokines, the increase in AT2 and the presence of antiphospholipid antibodies are known factors for TF activation and overexpression. It is very likely that the overexpression of TF in COVID-19 may be related to the pathogenesis of the disease, hence the importance of knowing the aspects related to this protein and the therapeutic strategies that can be derived. Different therapeutic strategies are being built to curb the expression of TF as a therapeutic target for various prothrombotic events; therefore, analyzing this treatment strategy for COVID-19-associated coagulopathy is rational. Medications such as celecoxib, cyclosporine or colchicine can impact on COVID-19, in addition to its anti-inflammatory effect, through inhibition of TF.

Indexed as

COVID-19 Drug TreatmentAngiotensin-Converting Enzyme 2CelecoxibColchicineCOVID-19CyclosporineCytokinesHumansSARS-CoV-2ThromboplastinACE2 protein, humanAngiotensin-Converting Enzyme 2CelecoxibColchicineCyclosporineCytokinesThromboplastincoagulopathyCOVID-19Covid-2-associated coagulopathySARS-CoV-2thrombosistissue factor

Identifiers

PMID33784877
PMCPMC8020089
OpenAlexW3146523107

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.