ArticleFrontiers in immunology2025
NF-κB/IL-6 axis drives impaired corneal wound healing in aqueous-deficient dry eye.
Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed.
- Research progress in animal models of dry eye disease: Types, mechanisms, and application prospects.Animal models and experimental medicine · 2026Review
- T-LysYal for Managing Dry Eye Disease, the Advent of Supramolecular Aggregates in Ophthalmology: A Narrative Review.Journal of clinical medicine · 2026Review
- Bisphenol A exacerbates dry eye disease via the CASP1/GSDMD-mediated pyroptotic axis: network toxicology, mendelian randomization, and experimental validation.Frontiers in pharmacology · 2026Article
- Correlation between tear cytokine profiles and corneal injury degree in patients with dry eye syndrome.Frontiers in immunology · 2026Article
- Platelet-Derived Growth Factor Isoform Imbalance Is Associated with Innate Inflammation and Corneal Epitheliopathy in Dry Eye Disease.Ophthalmic research · 2026Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dry eye disease (DED) commonly leads to compromised corneal epithelial integrity and chronic ocular surface inflammation; however, the precise molecular mechanisms underlying impaired corneal healing remain incompletely understood. In this study, we established an aqueous-deficient DED mouse model via extraorbital lacrimal gland excision (LGE) to investigate the cellular and molecular events contributing to delayed corneal repair following epithelial injury. Our results demonstrated significant delays in corneal re-epithelialization and nerve regeneration in aqueous-deficient mice, accompanied by increased infiltration of neutrophils and γδ T cells. Transcriptomic profiling revealed robust activation of NF-κB-dependent inflammatory signaling and IL-6 pathways, alongside marked suppression of genes associated with essential metabolic processes involved in tissue repair. Targeted pharmacological inhibition of NF-κB using caffeic acid phenethyl ester (CAPE), or neutralization of IL-6 via topical anti-IL-6 antibody administration, effectively attenuated immune cell infiltration, accelerated epithelial regeneration, and enhanced nerve recovery. Collectively, our findings suggest that NF-κB/IL-6 signaling plays a key role in sustaining inflammation that impairs corneal healing, and that targeting this axis partially improves epithelial and neural outcomes.
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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 Socratic graph.