Evidence map›Paper›PMID 34161337›Full record

ArticlePloS one2021

SARS-CoV-2 uses major endothelial integrin αvβ3 to cause vascular dysregulation in-vitro during COVID-19.

Danielle Nader, Nicola Fletcher, Gerard F Curley, Steven W Kerrigan

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

46 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
  2. Article
  3. Molecular mechanisms of SARS-CoV-2 entry: implications for biomedical strategies.Microbiology and molecular biology reviews : MMBR · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. The Functions of SARS-CoV-2 Receptors in Diabetes-Related Severe COVID-19.International journal of molecular sciences · 2024
    Review
  11. Integrin αProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Review
  14. Pulmonary fibrosis: A short- or long-term sequelae of severe COVID-19?Chinese medical journal pulmonary and critical care medicine · 2023
    Review
  15. Review
  16. Review
  17. Article
  18. Article
  19. Targeting integrin pathways: mechanisms and advances in therapy.Signal transduction and targeted therapy · 2023
    Review
  20. Article
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 2 institutions in 1 country.

Danielle NaderCardiovascular Infection Research Group, School of Pharmacy and Biomolecular Sciences, RCSI University of Medicine and Health Sciences, Royal College of Surgeons in Ireland, Dublin 2, Ireland.
Nicola FletcherSchool of Veterinary Medicine, Veterinary Science Centre, University College Dublin, Belfield, Dublin 4, Ireland.
Gerard F CurleyDepartment of Anaesthesia and Critical Care Medicine, RCSI University of Medicine and Health Sciences, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
Steven W KerriganCardiovascular Infection Research Group, School of Pharmacy and Biomolecular Sciences, RCSI University of Medicine and Health Sciences, Royal College of Surgeons in Ireland, Dublin 2, Ireland.ORCID 0000-0001-8945-5703
Royal College of Surgeons in Ireland · IEUniversity College Dublin · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The unprecedented global COVID-19 pandemic has prompted a desperate international effort to accelerate the development of anti-viral candidates. For unknown reasons, COVID-19 infections are associated with adverse cardiovascular complications, implicating that vascular endothelial cells are essential in viral propagation. The etiological pathogen, SARS-CoV-2, has a higher reproductive number and infection rate than its predecessors, indicating it possesses novel characteristics that infers enhanced transmissibility. A unique K403R spike protein substitution encodes an Arg-Gly-Asp (RGD) motif, introducing a potential role for RGD-binding host integrins. Integrin αVβ3 is widely expressed across the host, particularly in the endothelium, which acts as the final barrier before microbial entry into the bloodstream. This mutagenesis creates an additional binding site, which may be sufficient to increase SARS-CoV-2 pathogenicity. Here, we investigate how SARS-CoV-2 passes from the epithelium to endothelium, the effects of αVβ3 antagonist, Cilengitide, on viral adhesion, vasculature permeability and leakage, and also report on a simulated interaction between the viral and host protein in-silico.

Indexed as

Antigens, CDBinding SitesCaco-2 CellsCadherin 5CadherinsComputer SimulationCOVID-19Endothelium, VascularHost-Pathogen InteractionsHumansIntegrin alphaVbeta3Models, MolecularMutationPermeabilitySARS-CoV-2Snake VenomsAntigens, CDCadherin 5CadherinsCilengitideIntegrin alphaVbeta3Snake VenomsSpike Glycoprotein, Coronavirus

Identifiers

PMID34161337
PMCPMC8221465
OpenAlexW3176719069

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.