ReviewOpen heart2020
Thrombotic complications of COVID-19 may reflect an upregulation of endothelial tissue factor expression that is contingent on activation of endosomal NADPH oxidase.
Review in Open heart, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 5 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
43 citing papers in PubMed, 5 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Tissue factor in COVID-19-associated coagulopathy.Thrombosis research · 2022Pooled it
- COVID-19 (SARS-CoV-2) infection and thrombotic conditions: A systematic review and meta-analysis.European journal of clinical investigation · 2021Pooled it
- Hemorrhagic and ischemic stroke in patients with coronavirus disease 2019: incidence, risk factors, and pathogenesis - a systematic review and meta-analysis.F1000Research · 2021Pooled 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
- Viral Comorbidities Remodel Host Transcriptome and Redox Signaling in an NADPH Oxidase Isoform-Specific Manner.Viruses · 2026Review
- From Defense to Disease: NADPH Oxidase in Cellular Function and Dysregulation.Journal of immunology research · 2026Review
- Effects of oxidative stress on viral infections: an overview.Npj viruses · 2025Review
- Article
- Ebselen: A Review on its Synthesis, Derivatives, Anticancer Efficacy and Utility in Combating SARS-COV-2.Mini reviews in medicinal chemistry · 2024Review
- Inflammation and Venous Thromboembolism in Hospitalized Patients with COVID-19.Diagnostics (Basel, Switzerland) · 2023Article
- A perspective study of the possible impact of obeticholic acid against SARS-CoV-2 infection.Inflammopharmacology · 2023Review
- NOX2 and NOX5 are increased in cardiac microvascular endothelium of deceased COVID-19 patients.International journal of cardiology · 2023Article
- Neutrophil activation and neutrophil extracellular traps (NETs) in COVID-19 ARDS and immunothrombosis.European journal of immunology · 2023Review
- A predicted structure of NADPH Oxidase 1 identifies key components of ROS generation and strategies for inhibition.PloS one · 2023Article
- Direct endothelial ENaC activation mitigates vasculopathy induced by SARS-CoV2 spike protein.Frontiers in immunology · 2023Article
- Molecular Biomarker Identification Using a Network-Based Bioinformatics Approach That Links COVID-19 With Smoking.Bioinformatics and biology insights · 2023Article
- Molecular Mechanisms Related to Responses to Oxidative Stress and Antioxidative Therapies in COVID-19: A Systematic Review.Antioxidants (Basel, Switzerland) · 2022Review
- D,L-Lysine-Acetylsalicylate + Glycine (LASAG) Reduces SARS-CoV-2 Replication and Shows an Additive Effect with Remdesivir.International journal of molecular sciences · 2022Article
- Oxidative Stress-Related Mechanisms in SARS-CoV-2 Infections.Oxidative medicine and cellular longevity · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The high rate of thrombotic complications associated with COVID-19 seems likely to reflect viral infection of vascular endothelial cells, which express the ACE2 protein that enables SARS-CoV-2 to invade cells. Various proinflammatory stimuli can promote thrombosis by inducing luminal endothelial expression of tissue factor (TF), which interacts with circulating coagulation factor VII to trigger extrinsic coagulation. The signalling mechanism whereby these stimuli evoke TF expression entails activation of NADPH oxidase, upstream from activation of the NF-kappaB transcription factor that drives the induced transcription of the TF gene. When single-stranded RNA viruses are taken up into cellular endosomes, they stimulate endosomal formation and activation of NADPH oxidase complexes via RNA-responsive toll-like receptor 7. It is therefore proposed that SARS-CoV-2 infection of endothelial cells evokes the expression of TF which is contingent on endosomal NADPH oxidase activation. If this hypothesis is correct, hydroxychloroquine, spirulina (more specifically, its chromophore phycocyanobilin) and high-dose glycine may have practical potential for mitigating the elevated thrombotic risk associated with COVID-19.
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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.