ArticleCommunications biology2025
Upregulation of ferroptosis in glucocorticoids-induced posterior subcapsular cataracts.
Article in Communications biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- DNA methylation-mediated silencing of MALAT1 promotes dexamethasone-induced growth plate chondrocyte ferroptosis via miR-124-3p/LPCAT3.Journal of bioenergetics and biomembranes · 2026Article
- Human Crystallin Variation and Cataract.Investigative ophthalmology & visual science · 2026Review
- Lens aging and disease: Molecular mechanisms, functional consequences, and pharmacological implications.Progress in retinal and eye research · 2026Review
- Drug-induced cataract: a real-world study based on the food and drug administration adverse event reporting system database.Frontiers in medicine · 2026Article
- Stress-Induced Disruption of Circadian and Neuroimmune Networks in Lacrimal Glands Drives Dry Eye Pathogenesis.Investigative ophthalmology & visual science · 2025Article
- Decreased serum and local GPX4 and SLC7A11 expression correlates with disease severity in non-traumatic osteonecrosis of the femoral head.Journal of orthopaedic surgery and research · 2025Article
- Redefining cell death: ferroptosis as a game-changer in ophthalmology.Frontiers in immunology · 2025Review
Corrections and comments
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Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Glucocorticoid-induced posterior subcapsular cataracts (GIC) is a common complication of patients received glucocorticoid treatment in clinic. We find that dexamethasone (DEX) induces lens epithelial cells' ferroptosis. DEX treatment increases intracellular ferroptosis signatures in lens epithelial cell line in vitro as well as in rat lens in vivo. The inhibition of ferroptosis by liproxstatin-1 reduces the incidence of DEX-induced rat GIC. Experimental evidence and expression profiling showed that DEX induces ferroptosis through upregulating tetraspanin CD82- controlled P53 expression. DEX-activated glucocorticoid receptors directly bind to the CD82 promoter, driving its transcriptional upregulation. CD82 expression is upregulated in the anterior capsular epithelium of GIC patients as well as in the DEX-treated rat lens and caused the cell death of anterior capsule. DEX treatment and Overexpression of CD82 in cells recapitulated ferroptotic signatures through P53 activation and GPX4/SLC7A11 suppression. Taken together, GIC is closely associated with the upregulation of CD82-P53-GPX4/SLC7A11 axis-mediated ferroptosis.
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Registered trials
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