ReviewInternational journal of molecular sciences2015
An Updated Review on the Genetics of Primary Open Angle Glaucoma.
Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
61 citing papers in PubMed, 1 synthesis or guideline pooled it, 116 citations in OpenAlex.
- Associations between TLR4 Polymorphisms and Open Angle Glaucoma: A Meta-Analysis.BioMed research international · 2019Pooled it
- Association of endothelial nitric oxide synthase (NOS3) gene polymorphisms with primary open-angle glaucoma in a Saudi cohort.PloS one · 2020Trial
- Association of FunctionalInternational journal of molecular sciences · 2026Article
- GGAs: Regulation of Multiple Sorting Pathways and Potential Association With Human Diseases.Journal of cellular and molecular medicine · 2026Review
- Genetic Risk Factors and Clinical Implications of Glaucoma in the Saudi Population: A Review.International journal of molecular sciences · 2026Review
- The Ocular and Gut Microbiome Axis in Understanding Glaucoma: A Systematic Review.Journal of clinical medicine · 2026Review
- Genetic Architecture and Clinical Phenotypes of Primary Open-Angle Glaucoma: An Updated Review of Mendelian Genes, GWAS Loci, and Polygenic Risk.Clinical ophthalmology (Auckland, N.Z.) · 2026Review
- Emerging role of epigenetic mechanisms in glaucoma and their translational potential.Frontiers in genetics · 2026Review
- Rho Kinase (ROCK) Inhibitors in the Treatment of Glaucoma and Glaucoma Surgery: A Systematic Review of Early to Late Phase Clinical Trials.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Review
- Single-nucleotide polymorphisms ofExperimental biology and medicine (Maywood, N.J.) · 2023Article
- Article
- Article
- Signatures of genetic variation in human microRNAs point to processes of positive selection and population-specific disease risks.Human genetics · 2022Article
- Matrix Metalloproteinases and Glaucoma.Biomolecules · 2022Review
- Recent developments of neuroprotective agents for degenerative retinal disorders.Neural regeneration research · 2022Review
- Asian Race and Primary Open-Angle Glaucoma: Where Do We Stand?Journal of clinical medicine · 2022Review
- Significance of the lncRNAs MALAT1 and ANRIL in occurrence and development of glaucoma.Journal of clinical laboratory analysis · 2022Article
- Evaluating TNF-α and Interleukin-2 (IL-2) Levels in African American Primary Open-Angle Glaucoma Patients.Genes · 2021Article
- Analysis of risk allele frequencies of single nucleotide polymorphisms related to open-angle glaucoma in different ethnic groups.BMC medical genomics · 2021Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiological studies suggest that by 2020 the prevalence of primary open angle glaucoma (POAG) is estimated to increase to 76.0 million, and to 111.8 million by 2040 globally due to the population aging. The prevalence of POAG is the highest among those of African descent, followed by Asians, and the lowest in Europeans. POAG is a genetically complex trait with a substantial fraction exhibiting a significant heritability. Less than 10% of POAG cases in the general population are caused by specific gene mutations and the remaining cases are polygenic. Quantitative traits related to POAG pathogenesis such as intra-ocular pressure (IOP), vertical cup/disc ratio (VCDR), optic disc area, and central corneal thickness (CCT) are highly heritable, and likely to be influenced at least in part by genes and show substantial variation in human populations. Recent genome-wide association studies (GWAS) have identified several single nucleotide polymorphisms (SNPs) at different loci including CAV1/CAV2, TMCO1, CDKN2B-AS1, CDC7-TGFBR3, SIX1/SIX6, GAS7 and ATOH7 to be associated with POAG and its related quantitative traits (endophenotypes). The chapter provides a brief overview on the different GWAS and SNP association studies and their correlation with various clinical parameters important for POAG in the population worldwide, including the Middle East.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.