ReviewAging and disease2024
Aging, Cellular Senescence, and Glaucoma.
Review in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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
41 citing papers in PubMed, 58 citations in OpenAlex.
- Impaired regulatory T-cell-mediated immune tolerance promotes neurodegeneration in glaucoma.medRxiv : the preprint server for health sciences · 2026Article
- Pyrroloquinoline Quinone and NADPharmaceuticals (Basel, Switzerland) · 2026Review
- Pharmacological effect of rhCC16 on COPD: anti-senescence via the PI3K-AKT-mTOR pathway.Molecular and cellular biochemistry · 2026Article
- The Dual Role of Macroglia in Glaucoma: Deciphering the Contributions of Astrocytes and Müller Cells to Retinal Neurodegeneration and Neuroprotection.International journal of molecular sciences · 2026Review
- Hydroxysafflor Yellow A for Diabetic Retinopathy: A Critical Review of Retinal Neurovascular Mechanisms and Systemic-to-Ocular Pharmacokinetic Barriers.Antioxidants (Basel, Switzerland) · 2026Review
- The Molecular Basis of Ocular Aging: Mechanisms, Pathologies, and Emerging Therapeutics.Investigative ophthalmology & visual science · 2026Review
- RANKL Inhibition and the Risk of Ocular Hypertension and Primary Open-Angle Glaucoma.Investigative ophthalmology & visual science · 2026Observational
- Plasma-aqueous dual-fluid NEAT1/miR-93-5p axis may be involved in retinal ganglion cell degeneration in glaucoma: mechanistic dissection and diagnostic model construction.Scientific reports · 2026Article
- Mitophagy in ophthalmic pathologies: Molecular mechanisms and therapeutic implications.Medicine · 2026Review
- Review of Therapeutic Potential of Coenzyme Q10 in Ophthalmology: Focus on Age-Related Macular Degeneration, Glaucoma, and Retinitis Pigmentosa.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondria transplantation reduces intraocular pressure by improving mitochondrial function and remodeling trabecular meshwork.Journal of translational medicine · 2026Article
- Global burden and cross-country inequalities of age-related eye diseases from 1990 to 2021: a comprehensive analysis of temporal trends and socioeconomic disparities.Eye and vision (London, England) · 2026Article
- Long non-coding RNAs and accelerated aging in bipolar disorder.Neuroscience applied · 2026Review
- Autophagy in ocular diseases: from mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Epigenetics of glaucoma in the trabecular meshwork.Clinical epigenetics · 2025Review
- Extracellular Vesicles and Glaucoma: Opportunities and Challenges.Current eye research · 2025Review
- The drug discovery and therapeutic nano-strategies targeting cellular senescence.Materials today. Bio · 2025Review
- Aging and Corneal Nerve Health: Mechanisms of Degeneration and Emerging Therapies for the Cornea.Cells · 2025Review
- Integrated genomics reveals cellular senescence-driven molecular networks and immune crosstalk in myopia pathogenesis.Journal of cell communication and signaling · 2025Article
- How has global research on neural degeneration in glaucoma evolved from 1977 to 2025? A pioneering bibliometric insight into trends, impact, and future directions.International ophthalmology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is one of the most serious risk factors for glaucoma, and according to age-standardized prevalence, glaucoma is the second leading cause of legal blindness worldwide. Cellular senescence is a hallmark of aging that is defined by a stable exit from the cell cycle in response to cellular damage and stress. The potential mechanisms underlying glaucomatous cellular senescence include oxidative stress, DNA damage, mitochondrial dysfunction, defective autophagy/mitophagy, and epigenetic modifications. These phenotypes interact and generate a sufficiently stable network to maintain the cell senescent state. Senescent trabecular meshwork (TM) cells, retinal ganglion cells (RGCs) and vascular endothelial cells reportedly accumulate with age and stress and may contribute to glaucoma pathologies. Therapies targeting the suppression or elimination of senescent cells have been found to ameliorate RGC death and improve vision in glaucoma models, suggesting the pivotal role of cellular senescence in the pathophysiology of glaucoma. In this review, we explore the biological links between aging and glaucoma, specifically delving into cellular senescence. Moreover, we summarize the current data on cellular senescence in key target cells associated with the development and clinical phenotypes of glaucoma. Finally, we discuss the therapeutic potential of targeting cellular senescence for the management of glaucoma.
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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.