ArticleAging cell2024
Lens capsule advanced glycation end products induce senescence in epithelial cells: Implications for secondary cataracts.
Article in Aging cell, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- Trial
- Lens capsular accumulation of advanced glycation end products in eyes with intraocular lens dislocation.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2026Article
- Aging, oxidative stress, and cataracts: Therapeutic prospects and translational insights into peroxiredoxin 6.Progress in retinal and eye research · 2026Review
- Gene regulatory networks involved in activation of Notch signaling by AGEs in the pathogenesis of diabetic kidney disease.PloS one · 2026Article
- Melatonin alleviates ferroptosis in lens epithelial cells via regulating METTL14 expression.Iranian journal of basic medical sciences · 2026Article
- Global challenges for lens and cataract research.Frontiers in ophthalmology · 2026Article
- Lens epithelial cells senescence in cataract pathogenesis and emerging therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
- Matrix molecules associated with both regulation of inflammation and pathogenic outcomes associated with the surface of the lens in the eyes of EAU mice.Experimental eye research · 2025Article
- SIRT1 Prevents Lens Epithelial Cell Senescence During Age-Related Cataract via Regulating p66Shc.Aging cell · 2025Article
- Transcriptomic Analysis of Human Lens Epithelium Tissue With and Without Cataract Surgery: Uncovering Novel Pathways of Post-Surgical Lens Epithelium Remodeling.Investigative ophthalmology & visual science · 2025Article
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Emodin alleviates the damage to lens epithelial cells in diabetic cataract by repressing the p53-mediated ferroptosis pathway.International ophthalmology · 2025Article
- Unanswered questions regarding the pathogenesis of late onset posterior capsular opacification.Frontiers in ophthalmology · 2025Review
- Lens capsule advanced glycation end products induce senescence in epithelial cells: Implications for secondary cataracts.Aging cell · 2024Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Posterior capsule opacification (PCO) is a common complication after cataract surgery. Residual lens epithelial cells (LECs) on the anterior lens capsule, after cataract surgery, migrate to the posterior lens capsule and undergo transdifferentiation into myofibroblast-like cells. Those cells synthesize excessive amounts of extracellular matrix and contribute to fibrosis during PCO. Cellular senescence, a phenomenon that increases with aging, has been implicated in several fibrotic diseases. Here, we have investigated the prevalence of senescent LECs within the lens posterior capsule and the ability of advanced glycation end products (AGEs) in lens capsules to induce senescence, contributing to PCO. Aged lens capsules from pseudophakic human cadaver eyes showed the presence of senescent LECs. In human capsular bags, LECs showed an age-dependent increase in senescence after 28 days of culture. Human LECs cultured on aged lens capsules for 3 days underwent senescence; this effect was not seen in LECs cultured on young lens capsules. Human LECs cultured on an AGE-modified extracellular matrix (ECM-AGEs) showed an AGE-concentration-dependent increase in the expression of senescence markers and reactive oxygen species (ROS) levels. Treatment with a RAGE antagonist and ROS inhibitor reduced the expression of senescence and fibrotic markers. Additionally, conditioned media from ECM-AGEs-treated cells induced the expression of fibrotic markers in naïve LECs. Together, these suggest that AGEs in the capsule induce senescence of LECs, which triggers the mesenchymal transition of neighboring non-senescent LECs and contributes to PCO.
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