ArticleAging cell2016
AGEs in human lens capsule promote the TGFβ2-mediated EMT of lens epithelial cells: implications for age-associated fibrosis.
Article in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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
42 citing papers in PubMed, 70 citations in OpenAlex.
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- Reversal of protein chemical aging by enzymatic deglycation.Nature communications · 2026Article
- 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
- Global challenges for lens and cataract research.Frontiers in ophthalmology · 2026Article
- 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
- 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
- Glycative stress as a cause of macular degeneration.Progress in retinal and eye research · 2024Review
- Pantothenate Kinase 4 Governs Lens Epithelial Fibrosis by Negatively Regulating Pyruvate Kinase M2-Related Glycolysis.Aging and disease · 2023Article
- Comparative proteomics in captive giant pandas to identify proteins involved in age-related cataract formation.Scientific reports · 2023Article
- Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway.Bioengineered · 2022Article
- Status of higher TGF-β1 and TGF-β2 levels in the aqueous humour of patients with diabetes and cataracts.BMC ophthalmology · 2022Article
- LncRNA GAS5 regulates migration and epithelial-to-mesenchymal transition in lens epithelial cells via the miR-204-3p/TGFBR1 axis.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Lens Fibrosis: Understanding the Dynamics of Cell Adhesion Signaling in Lens Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2022Review
- The local wound environment is a key determinant of the outcome of TGFβ signaling on the fibrotic response of CD44Experimental eye research · 2021Article
- Aging of the Retina: Molecular and Metabolic Turbulences and Potential Interventions.Annual review of vision science · 2021Review
- Article
- Advanced glycation end products in human diabetic lens capsules.Experimental eye research · 2021Article
- Protein posttranslational modification (PTM) by glycation: Role in lens aging and age-related cataractogenesis.Experimental eye research · 2021Review
- Knockout RAGE alleviates cardiac fibrosis through repressing endothelial-to-mesenchymal transition (EndMT) mediated by autophagy.Cell death & disease · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
Abstract
Proteins in basement membrane (BM) are long-lived and accumulate chemical modifications during aging; advanced glycation endproduct (AGE) formation is one such modification. The human lens capsule is a BM secreted by lens epithelial cells. In this study, we have investigated the effect of aging and cataracts on the AGE levels in the human lens capsule and determined their role in the epithelial-to-mesenchymal transition (EMT) of lens epithelial cells. EMT occurs during posterior capsule opacification (PCO), also known as secondary cataract formation. We found age-dependent increases in several AGEs and significantly higher levels in cataractous lens capsules than in normal lens capsules measured by LC-MS/MS. The TGFβ2-mediated upregulation of the mRNA levels (by qPCR) of EMT-associated proteins was significantly enhanced in cells cultured on AGE-modified BM and human lens capsule compared with those on unmodified proteins. Such responses were also observed for TGFβ1. In the human capsular bag model of PCO, the AGE content of the capsule proteins was correlated with the synthesis of TGFβ2-mediated α-smooth muscle actin (αSMA). Taken together, our data imply that AGEs in the lens capsule promote the TGFβ2-mediated fibrosis of lens epithelial cells during PCO and suggest that AGEs in BMs could have a broader role in aging and diabetes-associated fibrosis.
Indexed as
Identifiers
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.