ArticleBiochimica et biophysica acta2014
Selenite cataracts: activation of endoplasmic reticulum stress and loss of Nrf2/Keap1-dependent stress protection.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- Curcumin Nanoemulsion: Characterization and Effect on Cataracts in an In Vivo Animal Model and Ex Vivo Human Model.Biomolecules · 2026Article
- Crosstalk between endoplasmic reticulum stress and mitochondrial homeostasis: A new perspective on ophthalmic disease treatment.Journal of cell communication and signaling · 2026Review
- Aging of the human eye lens: Epigenetic landscape and therapeutic targets in age‑related cataracts (Review).International journal of molecular medicine · 2025Review
- Characteristic visual phenotypes in Korean wild mice (KWM/Hym).Laboratory animal research · 2024Article
- Oxidative Stress in Cataract Formation: Is There a Treatment Approach on the Horizon?Antioxidants (Basel, Switzerland) · 2024Review
- Minimizing Oxidative Stress in the Lens: Alternative Measures for Elevating Glutathione in the Lens to Protect against Cataract.Antioxidants (Basel, Switzerland) · 2024Review
- Antioxidant System and Endoplasmic Reticulum Stress in Cataracts.Cellular and molecular neurobiology · 2023Review
- Endoplasmic reticulum stress: molecular mechanism and therapeutic targets.Signal transduction and targeted therapy · 2023Review
- Redox Regulation in Age-Related Cataracts: Roles for Glutathione, Vitamin C, and the NRF2 Signaling Pathway.Nutrients · 2023Review
- Anticataract Effect of the Aqueous Extract of the Flowers ofAdvances in pharmacological and pharmaceutical sciences · 2023Article
- Potential Properties of Natural Nutraceuticals and Antioxidants in Age-Related Eye Disorders.Life (Basel, Switzerland) · 2022Review
- Senescence marker protein30 protects lens epithelial cells against oxidative damage by restoring mitochondrial function.Bioengineered · 2022Article
- Changes in DNA methylation hallmark alterations in chromatin accessibility and gene expression for eye lens differentiation.Epigenetics & chromatin · 2022Article
- Acetyl-11-Keto-Beta Boswellic Acid (AKBA) Protects Lens Epithelial Cells Against HFrontiers in pharmacology · 2022Article
- Aged Nrf2-Null Mice Develop All Major Types of Age-Related Cataracts.Investigative ophthalmology & visual science · 2021Article
- The Protective Effects of Flavonoids in Cataract Formation through the Activation of Nrf2 and the Inhibition of MMP-9.Nutrients · 2020Review
- Proteomics Study of Peripheral Blood Mononuclear Cells in Down Syndrome Children.Antioxidants (Basel, Switzerland) · 2020Article
- Biology of Inherited Cataracts and Opportunities for Treatment.Annual review of vision science · 2019Review
- CHOP is dispensable for lens transparency in wild-type and connexin50 mutant mice.Molecular vision · 2019Article
- Polyphenol-enriched fraction ofMolecular vision · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Cataract-induced by sodium selenite in suckling rats is one of the suitable animal models to study the basic mechanism of human cataract formation. The aim of this present investigation is to study the endoplasmic reticulum (ER) stress-mediated activation of unfolded protein response (UPR), overproduction of reactive oxygen species (ROS), and suppression of Nrf2/Keap1-dependent antioxidant protection through endoplasmic reticulum-associated degradation (ERAD) pathway and Keap1 promoter DNA demethylation in human lens epithelial cells (HLECs) treated with sodium selenite. Lenses enucleated from sodium selenite injected rats generated overproduction of ROS in lens epithelial cells and newly formed lens fiber cells resulting in massive lens epithelial cells death after 1-5days. All these lenses developed nuclear cataracts after 4-5days. Sodium selenite treated HLECs induced ER stress and activated the UPR leading to release of Ca(2+) from ER, ROS overproduction and finally HLECs death. Sodium selenite also activated the mRNA expressions of passive DNA demethylation pathway enzymes such as Dnmt1, Dnmt3a, and Dnmt3b, and active DNA demethylation pathway enzyme, Tet1 leading to DNA demethylation in the Keap1 promoter of HLECs. This demethylated Keap1 promoter results in overexpression of Keap1 mRNA and protein. Overexpression Keap1 protein suppresses the Nrf2 protein through ERAD leading to suppression of Nrf2/Keap1 dependent antioxidant protection in the HLECs treated with sodium selenite. As an outcome, the cellular redox status is altered towards lens oxidation and results in cataract formation.
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