ArticlePloS one2013
Mitochondrial genome analysis of primary open angle glaucoma patients.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Identifying potential key metabolic pathways and biomarkers in glaucoma: a systematic review and meta-analysis.BMJ open ophthalmology · 2025Pooled it
- Peripheral Blood Mononuclear Cell Oxygen Consumption and Systemic Bioenergetics in Glaucoma Management.International journal of molecular sciences · 2026Review
- Association between Nucleoside and Nucleotide Reverse Transcriptase Inhibitor Use and Primary Open-Angle Glaucoma Risk in All of Us.Ophthalmology · 2025Article
- Review
- Massively parallel sequencing of mitochondrial genome in primary open angle glaucoma identifies somatically acquired mitochondrial mutations in ocular tissue.Scientific reports · 2024Article
- Nicotinamide: Bright Potential in Glaucoma Management.Biomedicines · 2024Review
- Whole Exome Sequencing Reveals Novel Candidate Genes in Familial Forms of Glaucomatous Neurodegeneration.Genes · 2023Article
- Glial metabolic alterations during glaucoma pathogenesis.Frontiers in ophthalmology · 2023Review
- Paving the way while playing catch up: mitochondrial genetics in African ancestry primary open-angle glaucoma.Frontiers in ophthalmology · 2023Article
- Glaucoma diagnosis using multi-feature analysis and a deep learning technique.Scientific reports · 2022Article
- AMPK hyperactivation promotes dendrite retraction, synaptic loss, and neuronal dysfunction in glaucoma.Molecular neurodegeneration · 2021Article
- Discovery and clinical translation of novel glaucoma biomarkers.Progress in retinal and eye research · 2021Review
- Mitochondrial Genome Study Identifies Association Between Primary Open-Angle Glaucoma and Variants inFrontiers in genetics · 2021Article
- Mitochondrial DNA Variation and Disease Susceptibility in Primary Open-Angle Glaucoma.Investigative ophthalmology & visual science · 2018Article
- Glaucoma as a Metabolic Optic Neuropathy: Making the Case for Nicotinamide Treatment in Glaucoma.Journal of glaucoma · 2017Review
- Glaucoma: the retina and beyond.Acta neuropathologica · 2016Review
- Genetic association and stress mediated down-regulation in trabecular meshwork implicates MPP7 as a novel candidate gene in primary open angle glaucoma.BMC medical genomics · 2016Article
- Primary Open-Angle Glaucoma in Individuals of African Descent: A Review of Risk Factors.Journal of clinical & experimental ophthalmology · 2015Article
- Whole-mitochondrial genome sequencing in primary open-angle glaucoma using massively parallel sequencing identifies novel and known pathogenic variants.Genetics in medicine : official journal of the American College of Medical Genetics · 2015Article
- Measurement of Systemic Mitochondrial Function in Advanced Primary Open-Angle Glaucoma and Leber Hereditary Optic Neuropathy.PloS one · 2015Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary open angle glaucoma (POAG) is a multi-factorial optic disc neuropathy characterized by accelerating damage of the retinal ganglion cells and atrophy of the optic nerve head. The vulnerability of the optic nerve damage leading to POAG has been postulated to result from oxidative stress and mitochondrial dysfunction. In this study, we investigated the possible involvement of the mitochondrial genomic variants in 101 patients and 71 controls by direct sequencing of the entire mitochondrial genome. The number of variable positions in the mtDNA with respect to the revised Cambridge Reference Sequence (rCRS), have been designated "Segregating Sites". The segregating sites present only in the patients or controls have been designated "Unique Segregating Sites (USS)". The population mutation rate (θ = 4Neμ) as estimated by Watterson's θ (θw), considering only the USS, was significantly higher among the patients (p = 9.8 × 10(-15)) compared to controls. The difference in θw and the number of USS were more pronounced when restricted to the coding region (p<1.31 × 10(-21) and p = 0.006607, respectively). Further analysis of the region revealed non-synonymous variations were significantly higher in Complex I among the patients (p = 0.0053). Similar trends were retained when USS was considered only within complex I (frequency 0.49 vs 0.31 with p<0.0001 and mutation rate p-value <1.49×10(-43)) and ND5 within its gene cluster (frequency 0.47 vs 0.23 with p<0.0001 and mutation rate p-value <4.42×10(-47)). ND5 is involved in the proton pumping mechanism. Incidentally, glaucomatous trabecular meshwork cells have been reported to be more sensitive to inhibition of complex I activity. Thus mutations in ND5, expected to inhibit complex I activity, could lead to generation of oxidative stress and favor glaucomatous condition.
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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.