ArticleInvestigative ophthalmology & visual science2016
UV-A Irradiation Activates Nrf2-Regulated Antioxidant Defense and Induces p53/Caspase3-Dependent Apoptosis in Corneal Endothelial Cells.
Article in Investigative ophthalmology & visual science, 2016. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 101 citations in OpenAlex.
- The effect of diabetes on corneal endothelium: a meta-analysis.BMC ophthalmology · 2021Pooled it
- Metabolic and redox adaptations of the corneal endothelium: From metabolic plasticity to therapeutic opportunities.Redox biology · 2026Review
- PEDF Prevents Corneal Endothelial Dysfunction of Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Oxidative Stress in Keratoconus Is Evident in Tear Fluid and Stromal Cells and Alleviated in Cell Culture by Sulforaphane.Investigative ophthalmology & visual science · 2026Article
- A Cross-Species Hydroquinone Model Replicates Smoking-Related Corneal Endothelial Oxidative Injury and Enables Therapeutic Screening of FGF10.Investigative ophthalmology & visual science · 2026Article
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Oxidative-stress related increase in keratoconus tear MDA and GPX3 while NRF2-antioxidant functions decrease in stromal cells.bioRxiv : the preprint server for biology · 2025Article
- Centipede Polypeptide Affects the Inflammatory Reaction and Ferroptosis of Liver Cancer Cells Through the p53/TRAIL Pathway.Journal of cellular and molecular medicine · 2025Article
- Iron-Sulfur Clusters and Iron Responsive Element Binding Proteins Mediate Iron Accumulation in Corneal Endothelial Cells in Fuchs Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Review
- Autophagy-Enhancing Properties ofMolecules (Basel, Switzerland) · 2025Article
- Role of the transcription factor NRF2 in maintaining the integrity of the Blood-Brain Barrier.Fluids and barriers of the CNS · 2024Review
- Understanding the molecular mechanism of regeneration through apoptosis-induced compensatory proliferation studies - updates and future aspects.Apoptosis : an international journal on programmed cell death · 2024Review
- Idebenone Antagonizes P53-Mediated Neuronal Oxidative Stress Injury by Regulating CD38-SIRT3 Protein Level.Neurochemical research · 2024Article
- A grape-supplemented diet prevented ultraviolet (UV) radiation-induced cataract by regulating Nrf2 and XIAP pathways.The Journal of nutritional biochemistry · 2024Article
- Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.Aging · 2024Article
- Tanshinone Alleviates UVA-induced Melanogenesis in MelanocytesCurrent molecular medicine · 2024Article
- Mechanism and therapeutic potential of traditional Chinese medicine extracts in sepsis.Frontiers in pharmacology · 2024Review
- POLE2 Regulates Apoptosis of Oral Squamous Cell Carcinoma Cells through the PI3K/AKT Signaling Pathway.Current medical science · 2023Article
- Endoplasmic Reticulum Stress Disrupts Mitochondrial Bioenergetics, Dynamics and Causes Corneal Endothelial Cell Apoptosis.Investigative ophthalmology & visual science · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
purposeTo examine whether Nrf2-regulated antioxidant defense and p53 are activated in human corneal endothelial cells (CEnCs) by environmental levels of ultraviolet A (UV-A), a known stimulator of oxidative stress.
methodsImmortalized human CEnCs (HCEnCi) were exposed to UV-A fluences of 2.5, 5, 10, or 25 J/cm2, then allowed to recover for 3 to 24 hours. Control HCEnCi did not receive UV-A. Reactive oxygen species (ROS) were measured using H2DCFDA. Cell cytotoxicity was evaluated by lactate dehydrogenase (LDH) release. Levels of Nrf2, HO-1, NQO-1, p53, and caspase3 were detected by immunnoblotting or real-time PCR. Activated caspase3 was measured by immunoblotting and a fluorescence assay.
resultsExposure of HCEnCi to 5, 10, and 25 J/cm2 UV-A increased ROS levels compared with controls. Nrf2, HO-1, and NQO-1 mRNA increased 1.7- to 3.2-fold at 3 and 6 hours after irradiation with 2.5 and 5 J/cm2 UV-A. At 6 hours post irradiation, UV-A (5 J/cm2) enhanced nuclear Nrf2 translocation. At 24 hours post treatment, UV-A (5, 10, and 25 J/cm2) produced a 1.8- to 2.8-fold increase in phospho-p53 and a 2.6- to 6.0-fold increase in activated caspase3 compared with controls, resulting in 20% to 42% cell death.
conclusionsLower fluences of UV-A induce Nrf2-regulated antioxidant defense and higher fluences activate p53 and caspase3, indicating that even near-environmental levels of UV-A may affect normal CEnCs. This data suggest that UV-A may especially damage cells deficient in antioxidant defense, and thus may be involved in the etiology of Fuchs' endothelial corneal dystrophy (FECD).
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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.