ArticleFrontiers in neuroscience2019
Auranofin Mediates Mitochondrial Dysregulation and Inflammatory Cell Death in Human Retinal Pigment Epithelial Cells: Implications of Retinal Neurodegenerative Diseases.
Article in Frontiers in neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.
- Ferroptosis and ferritinophagy in diabetes complications.Molecular metabolism · 2022Pooled it
- Programmed cell death and risk of diabetic retinopathy: a Mendelian randomization study.Journal of translational medicine · 2026Article
- The role of NLRP3 inflammasome in age-related macular degeneration: mechanisms and therapeutic prospects.Frontiers in aging neuroscience · 2026Review
- Ferroptosis in diabetic retinopathy: from pathogenic mechanisms to translational prospects.Frontiers in endocrinology · 2026Review
- Acupuncture for retinitis pigmentosa: a comprehensive review.International ophthalmology · 2025Review
- Retinal Pigment Epithelium and Monocytes' Mitochondrial Control of Ferroptosis and its Relevance to Age-Related Macular Degeneration.Molecular neurobiology · 2025Article
- Flotillin- 1 ameliorates experimental diabetic retinopathy by inhibiting ferroptosis in blood-retinal barrier.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Article
- α1D Adrenergic Receptor Antagonism Protects Against High Glucose-Induced Mitochondrial Dysfunction and Blood Retinal Barrier Breakdown in ARPE-19 Cells.International journal of molecular sciences · 2025Article
- Redefining cell death: ferroptosis as a game-changer in ophthalmology.Frontiers in immunology · 2025Review
- TRAP1 Improves Diabetic Retinopathy by Preserving Mitochondrial Function.Clinical ophthalmology (Auckland, N.Z.) · 2025Article
- Review
- Non-Apoptotic Programmed Cell Death as Targets for Diabetic Retinal Neurodegeneration.Pharmaceuticals (Basel, Switzerland) · 2024Review
- USP48 deubiquitination stabilizes SLC1A5 to inhibit retinal pigment epithelium cell inflammation, oxidative stress and ferroptosis in the progression of diabetic retinopathy.Journal of bioenergetics and biomembranes · 2024Article
- MiR-204-5p may regulate oxidative stress in myopia.Scientific reports · 2024Article
- Alleviated NCOA4-mediated ferritinophagy protected RA FLSs from ferroptosis in lipopolysaccharide-induced inflammation under hypoxia.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- Ferroptosis and its emerging role in kidney stone formation.Molecular biology reports · 2024Review
- Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning.Molecular neurobiology · 2024Article
- The important role of ferroptosis in inflammatory bowel disease.Frontiers in medicine · 2024Review
- Ferroptosis: a novel mechanism of cell death in ophthalmic conditions.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposePhotoreceptor degeneration occurs in various retinal diseases including age-related macular degeneration (AMD), Retinitis pigmentosa (RP), and diabetic retinopathy (DR). However, molecular mechanisms are not fully understood yet. The retinal pigment epithelium (RPE) forms the outer blood retinal barrier (oBRB) and supplies glucose, oxygen and nutrients from the fenestrated choriocapillaris to photoreceptors for visual function. Therefore, RPE dysfunction leads to photoreceptor injury/death and progression of blinding eye diseases. This study aims to understand the role of the thioredoxin (Trx) and its reductase (TrxR) redox signaling in human RPE dysfunction and cell death mechanism(s) in an
methodsA human RPE cell line (APRE-19) was cultured in DMEM/F12 medium and treated with auranofin (AF - 4 μM, an inhibitor of TrxR) for 4 and 24 h. Mitochondrial and lysosomal function, cellular oxidative stress and NLRP3 inflammasome activity were measured using cell assays, Western blotting, and confocal microscopy. Antioxidants and anti-inflammatory compounds were tested for blocking AF effects on RPE damage. Cell death mechanisms (LDH release to culture media) were determined using necroptosis, ferroptosis and pyroptosis inhibitors.
resultsAuranofin causes mitochondrial dysfunction (Δψm↓ and ATP↓), oxidative stress (H
conclusionThe Trx/TrxR redox system is critical for RPE function and viability. We previously showed that thioredoxin-interacting protein (TXNIP) is strongly induced in DR inhibiting the Trx/TrxR system and RPE dysfunction. Therefore, our results suggest that the TXNIP-Trx-TrxR redox pathway may participate in RPE dysfunction in DR and other retinal neurodegenerative diseases.
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Registered trials
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