ArticleScientific reports2016
Continuous exposure to non-lethal doses of sodium iodate induces retinal pigment epithelial cell dysfunction.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 43 citations in OpenAlex.
- Ferroptosis modulation by Toxoplasma gondii suppresses sodium iodate-driven age-related macular degeneration.Genes & genomics · 2026Article
- Unveiling the non-linear synergistic effects of smoking and aging on cataract-AMD comorbidity: an explainable artificial intelligence approach.Frontiers in public health · 2026Article
- Physicochemical Stability and Cross-Context Validation of PEGylated Human Serum Albumin Nanoparticles for Dual Neurotrophin Delivery in the Rabbit Eye and Oxidative Stress Models.International journal of nanomedicine · 2026Article
- Retinal Pigment Epithelium and Monocytes' Mitochondrial Control of Ferroptosis and its Relevance to Age-Related Macular Degeneration.Molecular neurobiology · 2025Article
- Molecular Mechanisms of Epithelial-Mesenchymal Transition in Retinal Pigment Epithelial Cells: Implications for Age-Related Macular Degeneration (AMD) Progression.Biomolecules · 2025Review
- Rekindling Vision: Innovative Strategies for Treating Retinal Degeneration.International journal of molecular sciences · 2025Review
- Intravitreal Administration of Avacincaptad Pegol in a Nonhuman Primate Model of Dry Age-Related Macular Degeneration.Pharmacology research & perspectives · 2025Article
- The microRNA Let-7f Induces Senescence and Exacerbates Oxidative Stress in Retinal Pigment Epithelial Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Article
- Retinal debris triggers cytotoxic damage in cocultivated primary porcine RPE cells.Frontiers in neuroscience · 2024Article
- Impaired Immunomodulatory Properties of the Retina from the Inflammatory Environment of the Damaged Eye.Inflammation · 2023Article
- Evaluation of CRISPR/Cas9 exon-skipping vector for choroideremia using human induced pluripotent stem cell-derived RPE.The journal of gene medicine · 2023Article
- The impact of early RPE cell junction loss on VEGF, Ang-2, and TIMP secretion in vitro.Molecular vision · 2023Article
- Hypoxia aggravates ferroptosis in RPE cells by promoting the Fenton reaction.Cell death & disease · 2022Article
- Inhibition of DUSP6 Activates Autophagy and Rescues the Retinal Pigment Epithelium in Sodium Iodate-Induced Retinal Degeneration Models In Vivo and In Vitro.Biomedicines · 2022Article
- Release of Iron-Loaded Ferritin in Sodium Iodate-Induced Model of Age Related Macular Degeneration: An In-Vitro and In-Vivo Study.Antioxidants (Basel, Switzerland) · 2021Article
- Quercetin Alleviates the Accumulation of Superoxide in Sodium Iodate-Induced Retinal Autophagy by Regulating Mitochondrial Reactive Oxygen Species Homeostasis through Enhanced Deacetyl-SOD2 via the Nrf2-PGC-1α-Sirt1 Pathway.Antioxidants (Basel, Switzerland) · 2021Article
- Review
- Sodium iodate induces ferroptosis in human retinal pigment epithelium ARPE-19 cells.Cell death & disease · 2021Article
- The CD36 Ligand-Promoted Autophagy Protects Retinal Pigment Epithelial Cells from Oxidative Stress.Oxidative medicine and cellular longevity · 2021Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related macular degeneration (AMD), characterized by progressive degeneration of retinal pigment epithelium (RPE), is the major cause of irreversible blindness and visual impairment in elderly population. We previously established a RPE degeneration model using an acute high dose sodium iodate to induce oxidative stress. Here we report findings on a prolonged treatment of low doses of sodium iodate on human RPE cells (ARPE-19). RPE cells were treated continuously with low doses (2-10 mM) of sodium iodate for 5 days. Low doses (2-5 mM) of sodium iodate did not reduce RPE cell viability, which is contrasting to cell apoptosis in 10 mM treatment. These low doses are sufficient to retard RPE cell migration and reduced expression of cell junction protein ZO-1. Phagocytotic activity of RPE cells was attenuated by sodium iodate dose-dependently. Sodium iodate also increased expression of FGF-2, but suppressed expression of IL-8, PDGF, TIMP-2 and VEGF. Furthermore, HTRA1 and epithelial-to-mesenchymal transition marker proteins were downregulated, whereas PERK and LC3B-II proteins were upregulated after sodium iodate treatment. These results suggested that prolonged exposure to non-lethal doses of oxidative stress induces RPE cell dysfunctions that resemble conditions in AMD. This model can be used for future drug/treatment investigation on AMD.
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