ArticleFree radical biology & medicine2011
Overexpression of SOD in retina: need for increase in H2O2-detoxifying enzyme in same cellular compartment.
Article in Free radical biology & medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.
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Who cites it
55 citing papers in PubMed, 89 citations in OpenAlex.
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- Retinal Gatekeepers: Molecular Mechanism and Therapeutic Role of Cysteine and Selenocysteine.Biomolecules · 2025Review
- Mechanisms of Rhodopsin-Related Inherited Retinal Degeneration and Pharmacological Treatment Strategies.Cells · 2025Review
- The role of the KEAP1-NRF2 signaling pathway in form deprivation myopia guinea pigs.BMC ophthalmology · 2024Article
- Pathological high intraocular pressure induces glial cell reactive proliferation contributing to neuroinflammation of the blood-retinal barrier via the NOX2/ET-1 axis-controlled ERK1/2 pathway.Journal of neuroinflammation · 2024Article
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- Oxidative stress in the eye and its role in the pathophysiology of ocular diseases.Redox biology · 2023Review
- Identification of Biomarkers Affecting Cryopreservation Recovery Ratio in Ram Spermatozoa Using Tandem Mass Tags (TMT)-Based Quantitative Proteomics Approach.Animals : an open access journal from MDPI · 2023Article
- Mechanism of Cone Degeneration in Retinitis Pigmentosa.Cellular and molecular neurobiology · 2023Review
- Effects of Antioxidant Gene Overexpression on Stress Resistance and Malignization In Vitro and In Vivo: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Nutraceutical Molecules Slow Down Retinal Degeneration, in Tvrm4 Mice a Model of Retinitis Pigmentosa, by Genetic Modulation of Anti-oxidant Pathway.Frontiers in neuroscience · 2022Article
- Molecular Mechanisms of Iron Mediated Programmed Cell Death and Its Roles in Eye Diseases.Frontiers in nutrition · 2022Review
- Polydopamine nanoparticles attenuate retina ganglion cell degeneration and restore visual function after optic nerve injury.Journal of nanobiotechnology · 2021Article
- Mitigating the pro-oxidant state and melanogenesis of Retinitis pigmentosa: by counteracting mitochondrial dysfunction.Cellular and molecular life sciences : CMLS · 2021Review
- Modulation of SOD3 Levels Is Detrimental to Retinal Homeostasis.Antioxidants (Basel, Switzerland) · 2021Article
- Photoreceptor metabolic reprogramming: current understanding and therapeutic implications.Communications biology · 2021Review
- Oxidative Stress and Microglial Response in Retinitis Pigmentosa.International journal of molecular sciences · 2020Review
- Review
- Seminal Plasma Proteome as an Indicator of Sperm Dysfunction and Low Sperm Motility in Chickens.Molecular & cellular proteomics : MCP · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
In retinitis pigmentosa (RP), various mutations cause rod photoreceptor cell death leading to increased oxygen levels in the outer retina, progressive oxidative damage to cones, and gradual loss of cone cell function. We have been exploring the potential of overexpressing components of the endogenous antioxidant defense system to preserve cone cell function in rd10(+/+) mice, a model of RP. rd10(+/+) mice deficient in superoxide dismutase 1 (SOD1) showed increased levels of superoxide radicals and carbonyl adducts (a marker of oxidative damage) in the retina and more rapid loss of cone function than rd10(+/+) mice with normal levels of SOD1. This suggests that SOD1 is an important component of the antioxidant defense system of cones, but increased expression of SOD1 in rd10(+/+) mice increased oxidative damage and accelerated the loss of cone function. Coexpression of SOD1 with glutathione peroxidase 4 (Gpx4), which like SOD1 is localized in the cytoplasm, but not with catalase targeted to the mitochondria, reduced oxidative damage in the retina and significantly slowed the loss of cone cell function in rd10(+/+) mice. Gene transfer resulting in increased expression of SOD2, but not coexpression of SOD2 and mitochondrial Gpx4, resulted in high levels of H(2)O(2) in the retina. These data suggest that to provide benefit in RP, overexpression of an SOD must be combined with expression of a peroxide-detoxifying enzyme in the same cellular compartment.
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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.