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Updated: Jul 16, 2025

SA-β-Galactosidase-Based Screening Assay for the Identification of Senotherapeutic Drugs
Published on: June 28, 2019
Aging, Cellular Senescence, and Glaucoma
Yumeng Zhang1, Shouyue Huang1, Bing Xie1
1Department of Ophthalmology, Ruijin Hospital Affiliated Medical School, Shanghai Jiaotong University, Shanghai 200025, China.
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.
Insights
Cellular senescence, a hallmark of aging, contributes to glaucoma by damaging cells like trabecular meshwork and retinal ganglion cells. Targeting these senescent cells shows promise for treating glaucoma and preserving vision.
Area of Science:
- Ophthalmology
- Gerontology
- Cell Biology
Background:
- Aging is a primary risk factor for glaucoma, the second leading cause of legal blindness globally.
- Cellular senescence, characterized by stable cell cycle exit due to damage, is a key aging hallmark.
- Glaucoma pathogenesis involves cellular senescence in critical eye cells, including trabecular meshwork and retinal ganglion cells.
Purpose of the Study:
- To explore the biological links between aging and glaucoma, focusing on cellular senescence.
- To summarize current data on cellular senescence in glaucoma-associated cells.
- To discuss therapeutic strategies targeting cellular senescence for glaucoma management.
Main Methods:
- Review of existing literature on aging, cellular senescence, and glaucoma.
- Analysis of mechanisms contributing to glaucomatous cellular senescence (oxidative stress, DNA damage, etc.).
- Examination of senescent cell accumulation in trabecular meshwork, retinal ganglion cells, and vascular endothelial cells.
Main Results:
- Cellular senescence, driven by factors like oxidative stress and mitochondrial dysfunction, plays a significant role in glaucoma.
- Accumulation of senescent cells in key ocular tissues contributes to glaucoma pathology.
- Therapies eliminating senescent cells have shown potential in improving vision and reducing retinal ganglion cell death in glaucoma models.
Conclusions:
- Cellular senescence is a critical factor in the aging-related development and progression of glaucoma.
- Targeting senescent cells offers a promising therapeutic avenue for managing glaucoma.
- Further research into senolytics could lead to novel treatments for vision preservation in glaucoma patients.
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