ReviewJournal of thrombosis and thrombolysis2020
Potential role for tissue factor in the pathogenesis of hypercoagulability associated with in COVID-19.
Review in Journal of thrombosis and thrombolysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 6 of them syntheses that pooled 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.
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.
Who cites it
60 citing papers in PubMed, 6 syntheses or guidelines pooled it, 100 citations in OpenAlex.
- Prophylactic anticoagulants for non-hospitalised people with COVID-19.The Cochrane database of systematic reviews · 2023Pooled it
- Endotheliopathy in Acute COVID-19 and Long COVID.International journal of molecular sciences · 2023Pooled it
- Tissue factor in COVID-19-associated coagulopathy.Thrombosis research · 2022Pooled it
- Tissue factor links inflammation, thrombosis, and senescence in COVID-19.Scientific reports · 2022Pooled it
- COVID-19 Pathophysiology Predicts That Ischemic Stroke Occurrence Is an Expectation, Not an Exception-A Systematic Review.Frontiers in neurology · 2020Pooled it
- Immunothrombosis in Acute Respiratory Dysfunction of COVID-19.Frontiers in immunologyPooled it
- Renin-angiotensin imbalance promotes excessive fibrin deposition through M2 macrophage-derived tissue factor expression in eosinophilic chronic rhinosinusitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- CD169Frontiers in cellular and infection microbiology · 2026Article
- COVID-19 and acute limb ischemia: latest hypotheses of pathophysiology and molecular mechanisms.Journal of Zhejiang University. Science. B · 2025Review
- Sulfated Bile Acids in Serum as Potential Biomarkers of Disease Severity and Mortality in COVID-19.Cells · 2024Article
- Flow cytometry for extracellular vesicle characterization in COVID-19 and post-acute sequelae of SARS-CoV-2 infection.Extracellular vesicles and circulating nucleic acids · 2024Review
- Combined coagulation and inflammation markers as predictors of venous thrombo-embolism and death in COVID-19.Frontiers in medicine · 2024Article
- The Role of Tissue Factor In Signaling Pathways of Pathological Conditions and Angiogenesis.Current molecular medicine · 2024Review
- Epidemiology, pathogenesis, and management of Coronavirus disease 2019-associated stroke.Frontiers of medicine · 2023Review
- Crosstalk between Platelets and SARS-CoV-2: Implications in Thrombo-Inflammatory Complications in COVID-19.International journal of molecular sciences · 2023Review
- Review
- The effects of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on ischemic stroke and the possible underlying mechanisms.The International journal of neuroscience · 2023Article
- Rationale for combined therapies in severe-to-critical COVID-19 patients.Frontiers in immunology · 2023Review
- Estrogens as a Possible Therapeutic Strategy for the Management of Neuroinflammation and Neuroprotection in COVID-19.Current neuropharmacology · 2023Article
- Symmetrical peripheral gangrene: potential mechanisms and therapeutic approaches in severe COVID-19.Frontiers in cardiovascular medicine · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.