Evidence map›Paper›PMID 20140222›Full record

ArticlePloS one2010

VAV2 and VAV3 as candidate disease genes for spontaneous glaucoma in mice and humans.

Keiko Fujikawa, Takeshi Iwata, Kaoru Inoue, Masakazu Akahori, Hanako Kadotani, Masahiro Fukaya, Masahiko Watanabe, Qing Chang, Edward M Barnett, Wojciech Swat

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.7field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 65 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Retina regeneration: lessons from vertebrates.Oxford open neuroscience · 2022
    Review
  9. MicroRNAs in the aqueous humor of patients with different types of glaucoma.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2021
    Article
  10. Article
  11. Article
  12. Role of animal models in glaucoma research.Neural regeneration research · 2020
    Article
  13. Article
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. An In Vitro Perfusion System to Enhance Outflow Studies in Mouse Eyes.Investigative ophthalmology & visual science · 2016
    Article
  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

10 authors at 4 institutions in 2 countries.

Keiko FujikawaDepartment of Pathology and Immunology, Hokkaido University Graduate School of Medicine, Sapporo, Japan. fujikawa@med.hokudai.ac.jp
Takeshi Iwata
Kaoru Inoue
Masakazu Akahori
Hanako Kadotani
Masahiro Fukaya
Masahiko Watanabe
Qing Chang
Edward M Barnett
Wojciech Swat
Hokkaido University · JPSapporo University · JPTokyo Medical Center · JPWashington University in St. Louis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGlaucoma is a leading cause of blindness worldwide. Nonetheless, the mechanism of its pathogenesis has not been well-elucidated, particularly at the molecular level, because of insufficient availability of experimental genetic animal models. METHODOLOGY/PRINCIPAL

findingsHere we demonstrate that deficiency of Vav2 and Vav3, guanine nucleotides exchange factors for Rho guanosine triphosphatases, leads to an ocular phenotype similar to human glaucoma. Vav2/Vav3-deficient mice, and to a lesser degree Vav2-deficient mice, show early onset of iridocorneal angle changes and elevated intraocular pressure, with subsequent selective loss of retinal ganglion cells and optic nerve head cupping, which are the hallmarks of glaucoma. The expression of Vav2 and Vav3 tissues was demonstrated in the iridocorneal angle and retina in both mouse and human eyes. In addition, a genome-wide association study screening glaucoma susceptibility loci using single nucleotide polymorphisms analysis identified VAV2 and VAV3 as candidates for associated genes in Japanese open-angle glaucoma patients. CONCLUSIONS/SIGNIFICANCE: Vav2/Vav3-deficient mice should serve not only as a useful murine model of spontaneous glaucoma, but may also provide a valuable tool in understanding of the pathogenesis of glaucoma in humans, particularly the determinants of altered aqueous outflow and subsequent elevated intraocular pressure.

Indexed as

Genetic Predisposition to DiseaseAnimalsAntihypertensive AgentsAsian PeopleEyeGlaucomaGlaucoma, Open-AngleHumansHydrophthalmosImmunohistochemistryIn Situ HybridizationIntraocular PressureJapanLatanoprostMiceMice, Inbred C57BLAntihypertensive AgentsLatanoprostProstaglandins F, SyntheticProto-Oncogene Proteins c-vavVAV2 protein, humanVav2 protein, mouseVAV3 protein, humanVav3 protein, mouse

Identifiers

PMID20140222
PMCPMC2816215
OpenAlexW2099122463

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.