Evidence map›Paper›PMID 24258795›Full record

ReviewJapanese journal of ophthalmology2014

Genetics of primary open angle glaucoma.

Mitsuko Takamoto, Makoto Araie

Abstract readReview
PubMed Publisher
In one paragraph

Review in Japanese journal of ophthalmology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 3% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 52 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Screening ofMolecular biology research communications · 2018
    Article
  6. A recurrent G367R mutation inInternational journal of ophthalmology · 2018
    Article
  7. Article
  8. Article
  9. Common polymorphisms of theBioscience reports · 2017
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. An Updated Review on the Genetics of Primary Open Angle Glaucoma.International journal of molecular sciences · 2015
    Review
  16. Article
  17. Article
  18. [Functional disorders in the chronological progression of glaucoma].Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2015
    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

2 authors at 2 institutions in 1 country.

Mitsuko TakamotoDepartment of Ophthalmology, School of Medicine, The University of Tokyo, Tokyo, Japan.
Makoto Araie
Kanto Central Hospital · JPThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Glaucoma is a neurodegenerative disease and one of the leading causes of irreversible blindness, affecting over 60 million people worldwide. At the present time, glaucoma is clinically defined, but the exact etiology is unknown. Genetic studies are one approach to identify the molecules and pathways involved in disease pathogenesis. Familial aggregation of primary open-angle glaucoma (POAG) has long been recognized, and the analysis of POAG families with a Mendelian inheritance form of this disease has been employed to identify multiple loci linked to them. Some causative genes, such as myocilin, optineurin and WD repeat domain 36, have been identified. However, most cases of POAG are considered to be a prevalent, multifactorial disorder. Several association studies have been conducted for candidate genes, and genome-wide association studies recently identified new susceptibility loci for POAG, namely, S1 RNA binding domain 1 region on chromosome 2p21, the caveolin 1 and caveolin 2 regions on 7q31, transmembrane and coiled-coil domain 1 region on 1q24, cyclin-dependent kinase inhibitor 2B antisense RNA on 9p21, the SIX1 and SIX6 regions on 14q24 and, possibly, the regulatory region of 8q22. Further analysis of clinical manifestations caused by specific genes and functional analysis of these genes will contribute to the development of new strategies for the diagnosis and treatment of POAG.

Indexed as

Genetic LinkageGenetic Predisposition to DiseaseGenome-Wide Association StudyGlaucoma, Open-AngleHumans

Identifiers

PMID24258795
OpenAlexW2025448029

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.