ArticleAntioxidants (Basel, Switzerland)2025
Hyperosmolarity-Induced Oxidative Stress Leads to Senescence in Human Corneal Epithelial Cells (HCEPC) via DNA Damage, Metabolic Disturbance and Mitophagy Decline.
Article in Antioxidants (Basel, Switzerland), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Review
- Chrysin Attenuates Dry Eye Progression by Suppressing NOX2-Dependent Ferroptosis and STING/NLRP3-Mediated Inflammatory Responses.Investigative ophthalmology & visual science · 2026Article
- Honokiol Alleviates Dry Eye-Related Corneal Epithelial Damage by Activating SIRT3/PINK1-Mediated Mitophagy.Drug design, development and therapy · 2026Article
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Authors and funding
2 authors.
Funding
Abstract
backgroundDry eye disease (DED), characterized by tear film hyperosmolarity, can lead to corneal epithelial damage. The mechanisms linking hyperosmotic stress to human corneal epithelial cell (HCEPC) damage are not fully understood.
methodsA DED model was established by exposing HCEPCs to sustained hyperosmotic stress (400 mOsm/L) over multiple passages in vitro. Senescence was assessed using senescence-associated-β-galactosidase (SA-β-gal) staining, 5-ethynyl-2'-deoxyuridine (EdU) assays, p16
resultsHyperosmotic stress induced HCEPC senescence, driven by mitochondrial dysfunction, oxidative stress, DNA damage, bioenergetic crisis, and compromised autophagy (especially mitophagy). Autophagy and mitophagy play a key role in regulating senescence progression. Enhancing autophagy with LYN-1604 ameliorated oxidative stress, improved energy homeostasis, and attenuated senescence. Inhibiting autophagy exacerbated these states.
conclusionHyperosmolarity promotes HCEPC senescence via mitochondrial dysfunction and oxidative damage. Autophagy serves a critical protective role, and its enhancement represents a promising therapeutic strategy for DED.
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