ArticleInvestigative ophthalmology & visual science2025
Targeted Activation of OGG1 Inhibits Paraptosis in Lens Epithelial Cells of Early Age-Related Cortical Cataract.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Stimulation of OGG1 Enhances Oxidative DNA Damage Repair and Protects Against Acute Liver Failure by Acetaminophen.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Loss of Peroxiredoxin 6 Drives Age-Related Klf9/NF-Antioxidants (Basel, Switzerland) · 2026Article
- RNA sequencing and bioinformatics analysis of blood from patients with cortical cataracts.BMC ophthalmology · 2026Article
- OGG1 activation improves T cell resilience to oxidative stress after allo-SCT and T cell engager exposure.Leukemia · 2025Article
- Molecular Duality of OGG1: From Genomic Guardian to Redox-Sensitive Modulator in Diseases.Antioxidants (Basel, Switzerland) · 2025Review
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Authors and funding
10 authors.
Funding
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Abstract
Purpose: To investigate potential modes of programmed cell death in the lens epithelial cells (LECs) of patients with early age-related cortical cataract (ARCC) and to explore early-stage intervention strategies. Methods: Anterior lens capsules were collected from early ARCC patients for comprehensive analysis. Ultrastructural examination of LECs was performed using transmission electron microscopy. Cell death-associated protein markers were quantified via Western blot analysis, including those for paraptosis (ALIX, GRP78), apoptosis (cleaved caspase 3 and caspase 9), pyroptosis (N-GSDMD), and ferroptosis (GPX4). Intracellular vesicle-organelle colocalization was assessed through immunofluorescence. OGG1 protein expression and activity were evaluated through multiple methods, including Western blot, laser micro-irradiation, and immunofluorescence. The therapeutic potential of the OGG1 activator TH10785 on paraptosis was investigated using an ex vivo rat lens model. Results: Morphologic changes revealed significant endoplasmic reticulum (ER) swelling in ARCC patient LECs, with no characteristic apoptotic features. Paraptosis-related proteins exhibited significant alterations, while other cell death pathway markers (apoptosis, pyroptosis, and ferroptosis) remained unchanged. In the reactive oxygen species-induced paraptosis model, vesicular structures showed exclusive colocalization with ER-specific fluorescence. Elevated levels of the DNA damage marker 7,8-dihydro-8-oxoguanine were observed concurrent with decreased OGG1 activity. The OGG1 activator TH10785 showed efficacy in suppressing LECs paraptosis in ex vivo rat lens cultures. Conclusions: Paraptosis was identified in the LECs of patients with early ARCC. TH10785 activates OGG1 to suppress paraptosis in LECs, suggesting a novel therapeutic approach for early ARCC intervention.
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