ArticleAging cell2020
Early removal of senescent cells protects retinal ganglion cells loss in experimental ocular hypertension.
Article in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 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
44 citing papers in PubMed, 66 citations in OpenAlex.
- Historical Context for Cellular Senescence, Epigenetic Remodeling, and Lipid Metabolism in Ocular Aging.Investigative ophthalmology & visual science · 2026Article
- Dysregulation of neurovascular unit in the retina after optic nerve injury.BMC ophthalmology · 2026Article
- Lycium barbarum glycopeptide confers neuroprotection in chronic ocular hypertensive rats: a study investigating visual function, retinal structure, microcirculation, and pyroptosis.Frontiers in pharmacology · 2026Article
- Dasatinib and Quercetin Alleviate Retinal Ganglion Cell Dendritic Shrinkage and Promote Axonal Regeneration in Mice with Optic Nerve Injury.International journal of molecular sciences · 2025Article
- Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway.Molecular and cellular biochemistry · 2025Article
- Cytokines in age-related eye diseases: pathogenesis and potential targets for innovative therapies.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Aging-dependent YAP1 reduction contributes to AD pathology by upregulating the Nr4a1-AKT/GSK-3β axis.Translational neurodegeneration · 2025Article
- PRMT5 Regulates Senescence in Retinal Ganglion Cells by Targeting the Wnt/β-Catenin Signaling Cascade.Investigative ophthalmology & visual science · 2025Article
- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
- Aging and injury drive neuronal senescence in the dorsal root ganglia.Nature neuroscience · 2025Article
- Unraveling the immune response in optic nerve injury: implications for retinal ganglion cell protection.Frontiers in immunology · 2025Review
- Cellular senescence mediates retinal ganglion cell survival regulation post-optic nerve crush injury.Cell proliferation · 2024Article
- Anesthetic effects on electrophysiological responses across the visual pathway.Scientific reports · 2024Article
- Acute ocular hypertension in the living human eye: Model description and initial cellular responses to elevated intraocular pressure.Vision research · 2024Article
- Mendelian randomization implicates causal association between epigenetic age acceleration and age-related eye diseases or glaucoma endophenotypes.Clinical epigenetics · 2024Article
- Sirt6 protects retinal ganglion cells and optic nerve from degeneration during aging and glaucoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Modeling complex age-related eye disease.Progress in retinal and eye research · 2024Review
- Senolytic and senomorphic agent procyanidin C1 alleviates structural and functional decline in the aged retina.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Aging, Cellular Senescence, and Glaucoma.Aging and disease · 2024Review
- Computational identification of natural senotherapeutic compounds that mimic dasatinib based on gene expression data.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Experimental ocular hypertension induces senescence of retinal ganglion cells (RGCs) that mimics events occurring in human glaucoma. Senescence-related chromatin remodeling leads to profound transcriptional changes including the upregulation of a subset of genes that encode multiple proteins collectively referred to as the senescence-associated secretory phenotype (SASP). Emerging evidence suggests that the presence of these proinflammatory and matrix-degrading molecules has deleterious effects in a variety of tissues. In the current study, we demonstrated in a transgenic mouse model that early removal of senescent cells induced upon elevated intraocular pressure (IOP) protects unaffected RGCs from senescence and apoptosis. Visual evoked potential (VEP) analysis demonstrated that remaining RGCs are functional and that the treatment protected visual functions. Finally, removal of endogenous senescent retinal cells after IOP elevation by a treatment with senolytic drug dasatinib prevented loss of retinal functions and cellular structure. Senolytic drugs may have the potential to mitigate the deleterious impact of elevated IOP on RGC survival in glaucoma and other optic neuropathies.
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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 OpenQuestion graph.