ReviewClinical ophthalmology (Auckland, N.Z.)2015
Leber hereditary optic neuropathy: current perspectives.
Review in Clinical ophthalmology (Auckland, N.Z.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 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
105 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.
- Pooled it
- Trial
- Functional and structural analysis in relation to age at onset of Leber hereditary optic neuropathy: a Swedish cohort.Eye (London, England) · 2026Article
- Clinical features and temporal trends in a large Japanese LHON cohort, 1995-2024: a retrospective study.Eye (London, England) · 2026Article
- Mitochondrial genome microhomology-mediated editing by donor DNA delivery into mitochondria in human cells.Molecular therapy. Nucleic acids · 2026Article
- Mitochondrial complex I deficiency-associated diseases and models.Cellular and molecular life sciences : CMLS · 2026Review
- Optic nerve MRI findings in Leber's hereditary optic neuropathy.Japanese journal of ophthalmology · 2026Article
- Oxidative Stress and Inflammatory Biomarkers in Aqueous Humor and Blood of Patients with Leber's Hereditary Optic Neuropathy.Antioxidants (Basel, Switzerland) · 2025Article
- Review
- Review
- A viewpoint about Lenadogene nolparvovec failing to meet its primary endpoint even though it permanently corrects the m.11778G>A mutation causative of LHON.Eye (London, England) · 2025Article
- Evaluation of Visual and Optical Coherence Tomography Outcomes in Patients with Leber's Hereditary Optic Neuropathy Treated with Idebenone.Life (Basel, Switzerland) · 2025Article
- Article
- Remarkable visual improvement in Leber hereditary optic neuropathy.Japanese journal of ophthalmology · 2025Observational
- Isolated and Syndromic Genetic Optic Neuropathies: A Review of Genetic and Phenotypic Heterogeneity.International journal of molecular sciences · 2025Review
- Article
- Inhibition of cGMP-Signalling Rescues Retinal Ganglion Cells From Axotomy-Induced Degeneration.Journal of neurochemistry · 2025Article
- Article
- Autosomal Recessive Leber Hereditary Optic Neuropathy Triggered by Superior Mesenteric Artery Syndrome.Journal of neuro-ophthalmology : the official journal of the North American Neuro-Ophthalmology Society · 2025Article
- Age-Associated Differences in Optic Disc Findings of Leber's Hereditary Optic Neuropathy.Neuro-ophthalmology (Aeolus Press) · 2025Article
45 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 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Leber hereditary optic neuropathy (LHON) is one of the most common inherited optic neuropathies causing bilateral central vision loss. The disorder results from point mutations in mitochondrial DNA and subsequent mitochondrial dysfunction. The primary cell type that is lost in LHON is the retinal ganglion cell, which is highly susceptible to disrupted ATP production and oxidative stress. Inheritance of LHON follows that of mitochondrial genetics, and it has a highly variable clinical phenotype, as other genetic and environmental factors also play a role. Although LHON usually presents with isolated vision loss, some patients suffer other neurological sequelae. For ill-defined reasons, male LHON mutation carriers are more affected than females. Most LHON patients remain legally blind, but a small proportion can experience spontaneous partial recovery, often within the first year of symptom onset. Unfortunately, at this time there are no established curative interventions and treatment is largely supportive. Patients should be offered low vision services and counseled on mitigating risk factors for additional vision loss, such as smoking and consuming alcohol. Encouraging treatments currently undergoing investigation includes ubiquinone analogs, such as idebenone, as well as gene therapy and stem cells to restore ATP synthesis and provide neuroprotection to surviving retinal ganglion cells.
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.