ArticleInvestigative ophthalmology & visual science2025
Glutaredoxin 2 Protects Lens Epithelial Cells From Ferroptosis by Preventing HNRNPA2B1 S-Glutathionylation in Diabetes-Mediated Cataractogenesis.
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 1 paper.
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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.
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Who cites it
1 citing paper in PubMed.
- Repair of Corneal Epithelial Defects.Progress in molecular and subcellular biology · 2026Review
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The purpose of this study was to investigate the role of glutaredoxin 2 (Grx2) in regulating ferroptosis under oxidative stress conditions induced by high glucose in lens epithelial cells (LECs) and its potential contribution to diabetes-mediated cataractogenesis. Methods: Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to investigate proteins S-glutathionylation under high glucose condition, with validation by co-immunoprecipitation (Co-IP). Lentiviral transduction, Western blotting, FerroOrange, reactive oxygen species (ROS), and glutathione (GSH) measurements were applied to elucidate the downstream mechanisms. Results: High glucose-induced oxidative stress triggered ferroptosis in the LECs, thereby accelerating diabetes-mediated cataractogenesis. LC-MS/MS and Co-IP analysis identified HNRNPA2B1 as a Grx2-regulated target protein exhibiting increased glutathionylation. This modification regulated PTEN/AKT signaling, leading to mitochondrial dysfunction and subsequent ferroptosis induction. Conclusions: Grx2 exerts protective effects against ferroptosis in diabetes-mediated cataractogenesis by inhibiting HNRNPA2B1 S-glutathionylation and modulating PTEN/AKT signaling pathway.
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