Evidence map›Paper›PMID 22173078›Full record

ReviewEye (London, England)2012

Current concepts on primary open-angle glaucoma genetics: a contribution to disease pathophysiology and future treatment.

M Gemenetzi, Y Yang, A J Lotery

Open access · bronzeAbstract readReview
In one paragraph

Review in Eye (London, England), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 5 pooled it
10.4field-weighted citation impact, top 1% 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

53 citing papers in PubMed, 5 syntheses or guidelines pooled it, 120 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Pooled it
  6. Unsupervised Clustering for POAG Phenotyping.Investigative ophthalmology & visual science · 2026
    Article
  7. Gasotransmitters in Glaucoma: A New Paradigm.Bulletin of pharmaceutical research · 2026
    Article
  8. Primary open-angle glaucoma: a perspective from plasma metabolomics.Expert review of molecular diagnostics · 2025
    Review
  9. Article
  10. Article
  11. Observational
  12. Article
  13. Unmet needs in glaucoma therapy: The potential role of hydrogen sulfide and its delivery strategies.Journal of controlled release : official journal of the Controlled Release Society · 2022
    Review
  14. Visual field progression in Malay patients with primary glaucoma: survival analysis and prognostic factors.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022
    Article
  15. Review
  16. Article
  17. Review
  18. Review
  19. 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

3 authors at 3 institutions in 1 country.

M GemenetziSouthampton Eye Unit, Southampton General Hospital, Southampton, UK.
Y Yang
A J Lotery
Southampton General Hospital · GBUniversity of Southampton · GBWolverhampton Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma is a common, complex, heterogenous disease and it constitutes the major cause of irreversible blindness worldwide. Primary open-angle glaucoma (POAG) is the most common type of glaucoma in all populations. Most of the molecular mechanisms leading to POAG development are still unknown. Gene mutations in various populations have been identified by genetic studies and a genetic basis for glaucoma pathogenesis has been established. Linkage analysis and association studies are genetic approaches in the investigation of the genetic basis of POAG. Genome-wide association studies (GWAS) are more powerful compared with linkage analysis in discovering genes of small effect that might contribute to the development of the disease. POAG links to at least 20 genetic loci, but only 2 genes identified in these loci, myocilin and optineurin, are considered as well-established glaucoma-causing genes, whereas the role of other loci, genes, and variants implicated in the development of POAG remains controversial. Gene mutations associated with POAG result in retinal ganglion cell death, which is the common outcome of pathogenetic mechanisms in glaucoma. In future, if the sensitivity and specificity of genotyping increases, it may be possible to screen individuals routinely for disease susceptibility. This review is an update on the latest progress of genetic studies associated with POAG. It emphasizes the correlation of recent achievements in genetics with glaucoma pathophysiology, glaucoma treatment perspectives, and the possibility of future prevention of irreversible visual loss caused by the disease.

Indexed as

Genetic Predisposition to DiseaseChromosome MappingEye ProteinsGenome-Wide Association StudyGlaucoma, Open-AngleHumansEye Proteins

Identifiers

PMID22173078
PMCPMC3298987
OpenAlexW2042583371

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.