ArticleInvestigative ophthalmology & visual science2026
Inhibition of SGK1 Alleviates Apoptosis and Oxidative Stress in Dry Eye Disease by Activating FoxO3a-Mediated Autophagy.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: This study aimed to investigate the role of serum- and glucocorticoid-inducible kinase 1 (SGK1) in dry eye disease (DED) pathogenesis and its underlying molecular mechanisms. Methods: We established in vitro hyperosmotic models using human corneal epithelial cells (HCECs) and in vivo DED models induced by benzalkonium chloride in C57BL/6 mice. SGK1 was inhibited pharmacologically with GSK650394, and genetic knockdown of Forkhead box O3a (FoxO3a) was performed using small interfering RNA. Comprehensive assessments included western blot for apoptosis and autophagy markers, flow cytometry for apoptosis and reactive oxygen species (ROS) detection, mRFP-GFP-LC3 lentiviral transfection for autophagic flux monitoring, transmission electron microscopy for autophagic ultrastructure, co-immunoprecipitation for protein interactions, immunofluorescence staining for cellular localization, and histological examinations of ocular tissues. Results: SGK1 expression was significantly upregulated in both hyperosmotic-treated HCECs and the corneal epithelium of DED mice. SGK1 inhibition alleviated ocular surface damage, restored tear secretion, and reduced apoptosis and oxidative stress in vivo and in vitro. Mechanistically, SGK1 inhibition enhances autophagic flux by promoting FoxO3a nuclear translocation and activation, whereas FoxO3a knockdown abolishes the protective effects of SGK1 inhibition. Autophagy induction with rapamycin replicated the protective effects against DED-related damage. Conclusions: Inhibition of SGK1 alleviates apoptosis and oxidative stress in DED by activating FoxO3a-mediated autophagy. Our findings suggest that the SGK1/FoxO3a/autophagy axis may play a critical role in the pathogenesis of DED, and SGK1 may represent a potential therapeutic target for this condition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.