ArticleAging biology2023
Cellular senescence exacerbates features of aging in the eyes.
Article in Aging biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- The aging eye: navigating molecular mechanisms and innovative interventions.Biogerontology · 2026Review
- Influence of a Zombie-like State of the Liver on Drugs and Its Medico-Legal Implications: A Scoping Review.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Metabolic Dysfunction-Associated Steatotic Liver Disease Induced by Microplastics: An Endpoint in the Liver-Eye Axis.International journal of molecular sciences · 2025Review
- Advances in ocular aging: combining deep learning, imaging, and liquid biopsy biomarkers.Frontiers in medicine · 2025Review
- Age-Related Differences in the Mouse Corneal Epithelial Transcriptome and Their Impact on Corneal Wound Healing.Investigative ophthalmology & visual science · 2024Article
- Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.Aging · 2024Article
- Gene expression signatures of human senescent corneal and conjunctival epithelial cells.Aging · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Aging is a process often associated with various age-related diseases. Senescence is one of the hallmarks of aging, and senescent cells acquire a complex, often pro-inflammatory, secretory phenotype termed the senescence-associated secretory phenotype (SASP). Here we show that ocular surface cells from human cornea become senescent upon X-irradiation, characterized by increased SA-β-gal activity, decreased cell proliferation, increased expression of p16, and disruption of epithelial barrier. Comprehensive transcriptomic and proteomic analysis revealed that human senescent ocular cells acquire a SASP that disrupts epithelial barrier function. During aging in mice, senescent ocular cells accumulate, resulting in decreased epithelial barrier and chronic inflammation. Lacrimal gland excision, which leads to symptoms of dry eye (DE), resulted in corneal opacity associated with severe angiogenesis only in aged mice but not in young mice, and early senolytic treatment protected old DE mice from corneal opacity. In conclusion, senescent cells alter the ocular microenvironment through their SASP and eliminating these cells could represent a potential approach to alleviate symptoms associated with aged ocular surface.
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Registered trials
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