ArticleCell death & disease2021
Sodium iodate induces ferroptosis in human retinal pigment epithelium ARPE-19 cells.
Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 86 citations in OpenAlex.
- Ferroptosis in eye diseases: a systematic review.Eye (London, England) · 2025Pooled it
- Cisplatin-induced oxidative stress and ferroptosis-associated injury in retinal pigment epithelial cells attenuated by Toxoplasma gondii infection.Genes & genomics · 2026Article
- Ferroptosis modulation by Toxoplasma gondii suppresses sodium iodate-driven age-related macular degeneration.Genes & genomics · 2026Article
- Human retinal organoid model of disease-relevant photoreceptor cell death amenable to drug screening.Cell death & disease · 2026Article
- Formulation and evaluation of probucol-LCA nanoparticles for supressing oxidative stress-related retinal degeneration.Drug delivery and translational research · 2026Article
- Permeable nanoreactor eye drop for enzymatic cascade-mediated treatment for acute retinal injury model mimicking geographic atrophy.Nature communications · 2026Article
- Targeted Ferroptosis Improves RPE Phagocytosis via MERTK/NFE2L2/HMOX1 Axis to Alleviate Retinitis Pigmentosa.Investigative ophthalmology & visual science · 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
- CircAFF3 modulation of p53-ID2 signaling in the retinal pigment epithelium links inflammation with cell death in dry age-related macular degeneration.Frontiers in cell and developmental biology · 2026Article
- Mitochondrial outer membrane protein FUNDC2 contributes to ferroptosis as a potential upstream regulator in retinitis pigmentosa.International journal of ophthalmology · 2026Article
- Ferroptosis and the eye: bridging the gap between cell death and vision preservation.Frontiers in immunology · 2026Review
- iPLA2β Protects Retinal Pigment Epithelium From Ferroptosis in a Sodium Iodate-Induced Model of Dry AMD.Investigative ophthalmology & visual science · 2025Article
- Comparative transcriptomic analysis of retinal response to diverse cellular stresses reveals relative contributions of different cell death processes and signalling networks.Cell death & disease · 2025Article
- HDGF Protects Retinal Pigment Epithelium from Glyoxal-Induced Ferroptosis via SIRT1/PGC-1α/Nrf2 Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Targeting neurodegeneration and inflammation with thioredoxin-mimetic peptides.Redox biology · 2025Review
- Specific Assay Protocols for Porcine Single-Eye Retinal Pigment Epithelium Concerning Oxidative Stress and Inflammation.International journal of molecular sciences · 2025Article
- Retinal Gatekeepers: Molecular Mechanism and Therapeutic Role of Cysteine and Selenocysteine.Biomolecules · 2025Review
- The Role of Non-coding RNAs in Diabetic Retinopathy: Mechanistic Insights and Therapeutic Potential.Molecular neurobiology · 2025Review
- A PEDF-Derived Short Peptide Prevents Sodium Iodate-Induced Retinal Degeneration in Rats by Activating the SLC7A11/GSH/GPX4 Pathway in the RPE Cells.Journal of cellular and molecular medicine · 2025Article
- Intravenous Sodium Iodate Administration Induces Macula-Specific RPE Damage and Rod-Dominant Apoptosis in the Cynomolgus Monkey.Investigative ophthalmology & visual science · 2025Article
Corrections and comments
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sodium iodate (SI) is a widely used oxidant for generating retinal degeneration models by inducing the death of retinal pigment epithelium (RPE) cells. However, the mechanism of RPE cell death induced by SI remains unclear. In this study, we investigated the necrotic features of cultured human retinal pigment epithelium (ARPE-19) cells treated with SI and found that apoptosis or necroptosis was not the major death pathway. Instead, the death process was accompanied by significant elevation of intracellular labile iron level, ROS, and lipid peroxides which recapitulated the key features of ferroptosis. Ferroptosis inhibitors deferoxamine mesylate (DFO) and ferrostatin-1(Fer-1) partially prevented SI-induced cell death. Further studies revealed that SI treatment did not alter GPX4 (glutathione peroxidase 4) expression, but led to the depletion of reduced thiol groups, mainly intracellular GSH (reduced glutathione) and cysteine. The study on iron trafficking demonstrated that iron influx was not altered by SI treatment but iron efflux increased, indicating that the increase in labile iron was likely due to the release of sequestered iron. This hypothesis was verified by showing that SI directly promoted the release of labile iron from a cell-free lysate. We propose that SI depletes GSH, increases ROS, releases labile iron, and boosts lipid damage, which in turn results in ferroptosis in ARPE-19 cells.
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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 Socratic graph.