ArticleJournal of biomedical science2019
Reactive oxygen species-dependent mitochondrial dynamics and autophagy confer protective effects in retinal pigment epithelial cells against sodium iodate-induced cell death.
Article in Journal of biomedical science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 71 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Association between omega-6 fatty acids and diabetic retinopathy risk: a systematic review and meta-analysis.Nutrition & diabetes · 2026Pooled it
- AAV-based gene therapies for neovascular AMD.Gene therapy · 2026Review
- Tetrahydrocurcumin Attenuates NaIOAntioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial dynamics and their role in the pathogenesis of age-related macular degeneration: A comprehensive review.Redox biology · 2026Review
- Ferroptosis modulation by Toxoplasma gondii suppresses sodium iodate-driven age-related macular degeneration.Genes & genomics · 2026Article
- Mechanisms of Programmed Cell Death in Sodium Iodate-Driven Retinal Degeneration and the Role of DJ-1.International journal of molecular sciences · 2026Article
- Unveiling the choroidal immune landscape revealed interferon-gamma and TNF-alpha as novel therapeutic targets in dry AMD.Science China. Life sciences · 2026Article
- Role and regulation of kinases in age-related macular degeneration.Journal of translational medicine · 2026Review
- Time Course of Structural, Functional, Complement Changes and Inflammatory Processes in a Sodium Iodate Rat Model of Geographic Atrophy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Eriocitrin inhibits sodium iodate-induced cuproptosis and barrier function impairment in retinal pigment epithelium via SIRT7/YAP/ATP7A pathway.Journal of translational medicine · 2025Article
- Regulated cell death in age-related macular degeneration: Regulatory mechanisms and therapeutic potential.Journal of pharmaceutical analysis · 2025Review
- Regulatory role of serine 59 in the oligomeric dynamics and chaperone function of αB-crystallin.Scientific reports · 2025Article
- Hesperidin and Hesperetin from Orange Peel Water Extract Protect against NaIOJournal of agricultural and food chemistry · 2025Article
- MiR-21-5p promotes RPE cell necroptosis by targeting Peli1 in a rat model of AMD.In vitro cellular & developmental biology. Animal · 2025Article
- Cannabidiol-Loaded Retinal Organoid-Derived Extracellular Vesicles Protect Oxidatively Stressed ARPE-19 Cells.Biomedicines · 2025Article
- Artemisinin and Its Derivatives: Promising Therapeutic Agents for Age-Related Macular Degeneration.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Lamp2 Deficiency Enhances Susceptibility to Oxidative Stress-Induced RPE Degeneration.Investigative ophthalmology & visual science · 2025Article
- Retinal Pigment Epithelium Under Oxidative Stress: Chaperoning Autophagy and Beyond.International journal of molecular sciences · 2025Review
- Metabolomic profiling in a rat model of visual fatigue associated with liver-kidney yin deficiency syndrome.Frontiers in endocrinology · 2025Article
- Dihydromyricetin attenuates age-related macular degeneration: pharmacological effects and exploration of putative targets.Frontiers in pharmacology · 2025Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundOxidative stress is a major factor in retinal pigment epithelium (RPE) cells injury that contributes to age-related macular degeneration (AMD). NaIO3 is an oxidative toxic agent and its selective RPE cell damage makes it as a reproducible model of AMD. Although NaIO3 is an oxidative stress inducer, the roles of ROS in NaIO3-elicited signaling pathways and cell viability have not been elucidated, and the effect of NaIO3 on autophagy in RPE cells remains elusive.
methodsIn human ARPE-19 cells, we used Annexin V/PI staining to determine cell viability, immunoblotting to determine protein expression and signaling cascades, confocal microscopy to determine mitochondrial dynamics and mitophagy, and Seahorse analysis to determine mitochondrial oxidative phosphorylation.
resultsWe found that NaIO3 can dramatically induce cytosolic but not mitochondrial ROS production. NaIO3 can also activate ERK, p38, JNK and Akt, increase LC3II expression, induce Drp-1 phosphorylation and mitochondrial fission, but inhibit mitochondrial respiration. Confocal microscopic data indicated a synergism of NaIO3 and bafilomycin A1 on LC3 punctate formation, indicating the induction of autophagy. Using cytosolic ROS antioxidant NAC, we found that p38 and JNK are downstream signals of ROS and involve in NaIO3-induced cytotoxicity but not in mitochondrial dynamics, while ROS is also involved in LC3II expression. Unexpectedly NAC treatment upon NaIO3 stimulation leads to an enhancement of mitochondrial fragmentation and cell death. Moreover, inhibition of autophagy and Akt further enhances cell susceptibility to NaIO3.
conclusionsWe conclude that NaIO3-induced oxidative stress and cytosolic ROS production exert multiple signaling pathways that coordinate to control cell death in RPE cells. ROS-dependent p38 and JNK activation lead to cytotoxicity, while ROS-mediated autophagy and mitochondrial dynamic balance counteract the cell death mechanisms induced by NaIO3 in RPE 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 OpenQuestion graph.