ReviewJournal of optometry
A Review of Mitochondrial Optic Neuropathies: From Inherited to Acquired Forms.
Review in Journal of optometry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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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
27 citing papers in PubMed, 56 citations in OpenAlex.
- A Case Report of Late-Onset Leber's Hereditary Optic Neuropathy Diagnosed Following Vision Loss After Cataract Surgery.Neuro-ophthalmology (Aeolus Press) · 2026Article
- Mitochondrial PTRH2 controls the deubiquitinase TRABID to regulate mt-ND5 stability and metabolism.PNAS nexus · 2025Article
- The crossroads of Leber hereditary optic neuropathy and autosomal dominant optic Atrophy: Clinical profiles of patients with coexisting pathogenic genetic variants.American journal of ophthalmology case reports · 2025Article
- Article
- Macular OCT inner retinal changes reflect CNS involvement in m.3243A>G disease.BMJ neurology open · 2025Article
- Prophylactic nicotinamide treatment protects from rotenone-induced neurodegeneration by increasing mitochondrial content and volume.Acta neuropathologica communications · 2024Article
- Transient and Sustained Ganglion Cell Light Responses Are Differentially Modulated by Intrinsically Produced Reactive Oxygen Species Acting upon Specific Voltage-Gated NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Viability of mitochondria-labeled retinal ganglion cells in organotypic retinal explant cultures by two methods.Experimental eye research · 2023Article
- Posterior segment spectral domain oct in the differential diagnosis of bilateral temporal optic neuropathy and its correlation with visual acuity.International ophthalmology · 2022Article
- Wolfram Syndrome 1: From Genetics to Therapy.International journal of environmental research and public health · 2022Review
- Toxic and Nutritional Optic Neuropathies-An Updated Mini-Review.International journal of environmental research and public health · 2022Review
- Treatment of age-related visual impairment with a peptide acting on mitochondria.Disease models & mechanisms · 2022Article
- Clinical Overview of Leber Hereditary Optic Neuropathy.Acta medica Lituanic · 2022Review
- Characterisation of thickness changes in the peripapillary retinal nerve fibre layer in patients with Leber's hereditary optic neuropathy.The British journal of ophthalmology · 2021Article
- TGF-β2 Promotes Oxidative Stress in Human Trabecular Meshwork Cells by Selectively Enhancing NADPH Oxidase 4 Expression.Investigative ophthalmology & visual science · 2021Article
- Review
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- Review
- Mitochondrial Dysfunction as a Novel Target for Neuroprotective Nutraceuticals in Ocular Diseases.Nutrients · 2020Review
- A novel AFG3L2 mutation close to AAA domain leads to aberrant OMA1 and OPA1 processing in a family with optic atrophy.Acta neuropathologica communications · 2020Article
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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In recent years, the term mitochondrial optic neuropathy (MON) has increasingly been used within the literature to describe a group of optic neuropathies that exhibit mitochondrial dysfunction in retinal ganglion cells (RGCs). Interestingly, MONs include genetic aetiologies, such as Leber hereditary optic neuropathy (LHON) and dominant optic atrophy (DOA), as well as acquired aetiologies resulting from drugs, nutritional deficiencies, and mixed aetiologies. Regardless of an inherited or acquired cause, patients exhibit the same clinical manifestations with selective loss of the RGCs due to mitochondrial dysfunction. Various novel therapies are being explored to reverse or limit damage to the RGCs. Here we review the pathophysiology, clinical manifestations, differential diagnosis, current treatment, and promising therapeutic targets of MON.
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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.