ReviewPhilosophical transactions of the Royal Society of London. Series B, Biological sciences2011
The lens as a model for fibrotic disease.
Review in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 127 citations in OpenAlex.
- Assessment of candidate ocular biomarkers of ageing in a South African adult population: relationship with chronological age and systemic biomarkers.Mechanisms of ageing and developmentTrial
- Intracapsular metformin bioactivity and its role in posterior capsule opacification.The British journal of ophthalmology · 2026Article
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- Optical Quality Degradation Following Nd:YAG Laser-Induced Intraocular Lens Pitting: A Multimodal Experimental Study.Vision (Basel, Switzerland) · 2026Article
- Blockage of SUMO E1 enzyme inhibits ocular lens fibrosis by mediating SMAD4 SUMOylation.Genes & diseases · 2026Article
- Distinct transcriptional regulation of the Wnt and TGFβ signaling families associated with wound healing and fibrotic outcomes to lens injury.Experimental eye research · 2025Article
- Anterior Capsular Contraction Syndrome in Cataract Surgery: A Review of Challenges and Solutions.Medical science monitor : international medical journal of experimental and clinical research · 2025Review
- Supervised Machine-Based Learning and Computational Analysis to Reveal Unique Molecular Signatures Associated with Wound Healing and Fibrotic Outcomes to Lens Injury.International journal of molecular sciences · 2025Article
- Exosomes containing miR-148a-3p derived from mesenchymal stem cells suppress epithelial-mesenchymal transition in lens epithelial cells.Stem cells translational medicine · 2025Article
- Innovative Polymeric Biomaterials for Intraocular Lenses in Cataract Surgery.Journal of functional biomaterials · 2024Review
- Mefunidone Inhibits Inflammation, Oxidative Stress, and Epithelial-Mesenchymal Transition in Lens Epithelial Cells.Investigative ophthalmology & visual science · 2024Article
- TiO2-Nanoparticle-Enhanced Sonodynamic Therapy for Prevention of Posterior Capsular Opacification and Ferroptosis Exploration of Its Mechanism.Investigative ophthalmology & visual science · 2024Article
- Implications of Ocular Confounding Factors for Aqueous Humor Proteomic and Metabolomic Analyses in Retinal Diseases.Translational vision science & technology · 2024Article
- Transcriptome exploration of ferroptosis-related genes in TGFβ- induced lens epithelial to mesenchymal transition during posterior capsular opacification development.BMC genomics · 2024Article
- miR-26 Deficiency Causes Alterations in Lens Transcriptome and Results in Adult-Onset Cataract.Investigative ophthalmology & visual science · 2024Article
- Tonic ErbB signaling underlies TGFβ-induced activation of ERK and is required for lens cell epithelial to myofibroblast transition.Molecular biology of the cell · 2024Article
- miR-26 deficiency causes alterations in lens transcriptome and results in adult-onset cataract.bioRxiv : the preprint server for biology · 2024Article
- Application of transgenic mice to the molecular pathogenesis of cataract.International journal of ophthalmology · 2024Review
- miR-143 promotes cell proliferation, invasion and migration via directly binding to BRD2 in lens epithelial cells.American journal of translational research · 2024Article
- Pantothenate Kinase 4 Governs Lens Epithelial Fibrosis by Negatively Regulating Pyruvate Kinase M2-Related Glycolysis.Aging and disease · 2023Article
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis affects multiple organs and is associated with hyperproliferation, cell transdifferentiation, matrix modification and contraction. It is therefore essential to discover the key drivers of fibrotic events, which in turn will facilitate the development of appropriate therapeutic strategies. The lens is an elegant experimental model to study the processes that give rise to fibrosis. The molecular and cellular organization of the lens is well defined and consequently modifications associated with fibrosis can be clearly assessed. Moreover, the avascular and non-innervated properties of the lens allow effective in vitro studies to be employed that complement in vivo systems and relate to clinical data. Using the lens as a model for fibrosis has direct relevance to millions affected by lens disorders, but also serves as a valuable experimental tool to understand fibrosis per se.
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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.