ReviewInternational journal of molecular sciences2021
Mitochondrial Retinopathies.
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.
- Roles of mitochondrial fusion and fission in breast cancer progression: a systematic review.World journal of surgical oncology · 2022Pooled it
- The Oxidative-Mitochondrial-Inflammatory Axis in Retinitis Pigmentosa: Extracellular mtDNA as Biomarker and Therapeutic Read-Out.Antioxidants (Basel, Switzerland) · 2026Review
- Retinitis pigmentosa elicits neurodegeneration within the visual pathway in REEP6 knockout mice.Neural regeneration research · 2026Article
- Mitochondrial Genetic Diseases and Ophthalmic Manifestations: Molecular Pathophysiology, Genetics, and Clinical Management.International journal of molecular sciences · 2026Review
- Mitochondrial dysfunction in neurodegenerative disorders: mechanisms and therapeutic advances.Molecular biomedicine · 2026Review
- Intra-mitochondrial glycolysis maintains mitochondrial function and underlies the pathogenesis of retinitis pigmentosa.Nature communications · 2026Article
- Pituitary adenylate cyclase-activating polypeptide and mitochondrial homeostasis in neuronal injury: mechanisms and translational prospects.Frontiers in immunology · 2026Review
- Mitochondrial transfer and mesenchymal stem cells in ophthalmology: current evidence and therapeutic implications.Experimental biology and medicine (Maywood, N.J.) · 2026Review
- Absolute quantification of TCA cycle intermediates in mouse ocular tissues reveals distinct tissue- and sex-specific mitochondrial metabolism.bioRxiv : the preprint server for biology · 2025Article
- GW8510 alleviates muscle atrophy and skeletal muscle dysfunction in mice through AMPK/PGC1α signaling.International journal of molecular medicine · 2025Article
- Crucial Role of Early Detection in Managing Heart Failure in Kearns-Sayre Syndrome: A Case Report.The American journal of case reports · 2025Article
- Metabolic dysfunction promoted by mitochondrial DNA mutation burden drives retinal degeneration.bioRxiv : the preprint server for biology · 2025Article
- Role of mitochondria in physiological activities, diseases, and therapy.Molecular biomedicine · 2025Review
- Review
- Vitamin A treatment restores vision failures arising from Leber's hereditary optic neuropathy-linked mtDNA mutation.JCI insight · 2025Article
- Review
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Progressive mitochondrial dysfunction impairs visual signal transduction and induces retinal degeneration inFrontiers in insect science · 2025Article
- A Case of Late-Onset Leber's Hereditary Optic Neuropathy in Association with Heteroplasmic m.11778G>A/ND4 Mutation.Neuro-ophthalmology (Aeolus Press) · 2025Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The retina is an exquisite target for defects of oxidative phosphorylation (OXPHOS) associated with mitochondrial impairment. Retinal involvement occurs in two ways, retinal dystrophy (retinitis pigmentosa) and subacute or chronic optic atrophy, which are the most common clinical entities. Both can present as isolated or virtually exclusive conditions, or as part of more complex, frequently multisystem syndromes. In most cases, mutations of mtDNA have been found in association with mitochondrial retinopathy. The main genetic abnormalities of mtDNA include mutations associated with neurogenic muscle weakness, ataxia and retinitis pigmentosa (NARP) sometimes with earlier onset and increased severity (maternally inherited Leigh syndrome, MILS), single large-scale deletions determining Kearns-Sayre syndrome (KSS, of which retinal dystrophy is a cardinal symptom), and mutations, particularly in mtDNA-encoded ND genes, associated with Leber hereditary optic neuropathy (LHON). However, mutations in nuclear genes can also cause mitochondrial retinopathy, including autosomal recessive phenocopies of LHON, and slowly progressive optic atrophy caused by dominant or, more rarely, recessive, mutations in the fusion/mitochondrial shaping protein OPA1, encoded by a nuclear gene on chromosome 3q29.
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.