ArticleThe Journal of biological chemistry2019
Photoreceptors in a mouse model of Leigh syndrome are capable of normal light-evoked signaling.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Clarifying the composition of the ATP consumption factors required for maintaining ion homeostasis in mouse rod photoreceptors.Scientific reports · 2023Article
- Continuous Hypoxia Reduces Retinal Ganglion Cell Degeneration in a Mouse Model of Mitochondrial Optic Neuropathy.Investigative ophthalmology & visual science · 2022Article
- Article
- Noninvasive Ophthalmic Imaging Measures Retinal Degeneration and Vision Deficits in Ndufs4-/- Mouse Model of Mitochondrial Complex I Deficiency.Translational vision science & technology · 2022Article
- A proteogenomic signature of age-related macular degeneration in blood.Nature communications · 2022Article
- Retina Metabolism and Metabolism in the Pigmented Epithelium: A Busy Intersection.Annual review of vision science · 2021Review
- Progressive optic atrophy in a retinal ganglion cell-specific mouse model of complex I deficiency.Scientific reports · 2020Article
- Synaptic ribbons foster active zone stability and illumination-dependent active zone enrichment of RIM2 and Cav1.4 in photoreceptor synapses.Scientific reports · 2020Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction is an important cause of heritable vision loss. Mutations affecting mitochondrial bioenergetics may lead to isolated vision loss or life-threatening systemic disease, depending on a mutation's severity. Primary optic nerve atrophy resulting from death of retinal ganglion cells is the most prominent ocular manifestation of mitochondrial disease. However, dysfunction of other retinal cell types has also been described, sometimes leading to a loss of photoreceptors and retinal pigment epithelium that manifests clinically as pigmentary retinopathy. A popular mouse model of mitochondrial disease that lacks NADH:ubiquinone oxidoreductase subunit S4 (NDUFS4), a subunit of mitochondrial complex I, phenocopies many traits of the human disease Leigh syndrome, including the development of optic atrophy. It has also been reported that
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