Evidence map›Paper›PMID 32601125›Full record

ReviewClinical medicine (London, England)2020

Potential role of endothelial cell surface ectopic redox complexes in COVID-19 disease pathogenesis.

Isabella Panfoli

Open access · diamondAbstract readReview
In one paragraph

Review in Clinical medicine (London, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.7field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Review
  9. Review
  10. Review
  11. CanHeliyon · 2021
    Review
  12. Article
  13. Flagellar Hook Protein FlgE Induces Microvascular HyperpermeabilityFrontiers in cellular and infection microbiology · 2021
    Article
  14. Bioactive Lipids in COVID-19-Further Evidence.Archives of medical research · 2021
    Review
  15. Article
  16. Article
  17. Review
  18. Supplemental oxygen in COVID-19: a friend or foe?Clinical medicine (London, England) · 2020
    Article
  19. The Enigma of Endothelium in COVID-19.Frontiers in physiology · 2020
    Article
  20. COVID-19: A Challenge to Physiology of Aging.Frontiers in physiology · 2020
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Isabella PanfoliUniversity of Genoa, Genoa, Italy panfoli@difar.unige.it.
University of Genoa · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The novel coronavirus infectious disease (COVID-19) has rapidly spread and poses a great challenge to researchers, both in elucidating its pathogenic mechanism and developing effective treatments. It has been recently proposed that COVID-19 is an endothelial disease. Indeed, the COVID-19 virus binds to angiotensin-converting enzyme type 2 (ACE2), which is expressed in endothelial cells. ACE2 could be implicated in the production of reactive oxygen species (ROS) caused by endothelial dysfunction due to viral damage. Consequently, oxidative stress could prime these cells to acquire a pro-thrombotic and pro-inflammatory phenotype, predisposing patients to thromboembolic and vasculitic events and to disseminated intravascular coagulopathy (DIC). This implies a pivotal role played by oxygen in the pathogenetic mechanism of COVID-19 disease, in that its availability would tune the oxidant state and consequent damage.

Indexed as

Coronavirus InfectionsCOVID-19Disease ProgressionEndothelial CellsEndothelium, VascularHumansNeeds AssessmentPandemicsPneumonia, ViralRisk AssessmentSevere Acute Respiratory SyndromeSurvival AnalysisCOVID-19ectopic electron transfer chainendotheliumoxidative stressoxygen

Identifiers

PMID32601125
PMCPMC7539732
OpenAlexW3037292937

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.