ArticleThe American journal of pathology2017
Reduced Glutathione Level Promotes Epithelial-Mesenchymal Transition in Lens Epithelial Cells via a Wnt/β-Catenin-Mediated Pathway: Relevance for Cataract Therapy.
Article in The American journal of pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 57 citations in OpenAlex.
- Basement membrane remodeling with fibroblast activation and cystatin C aggregation in cerebral vessels of hereditary cystatin C amyloid angiopathy.Acta neuropathologica communications · 2026Article
- Paeonol suppresses epithelial-mesenchymal transition-driven posterior capsular opacification through activation of AMPK signaling.International journal of ophthalmology · 2026Article
- 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
- Macrophage-Hosted Porphyromonas gingivalis Is a Risk Factor for Cataract Development.Investigative ophthalmology & visual science · 2025Article
- The historical background of hereditary cystatin C amyloid angiopathy: Genealogical, pathological, and clinical manifestations.Brain pathology (Zurich, Switzerland) · 2025Review
- Mefunidone Inhibits Inflammation, Oxidative Stress, and Epithelial-Mesenchymal Transition in Lens Epithelial Cells.Investigative ophthalmology & visual science · 2024Article
- Oxidative Stress, Glutaredoxins, and Their Therapeutic Potential in Posterior Capsular Opacification.Antioxidants (Basel, Switzerland) · 2024Review
- Advances in Extracellular-Vesicles-Based Diagnostic and Therapeutic Approaches for Ocular Diseases.ACS nano · 2024Review
- Prevention of age-related truncation of γ-glutamylcysteine ligase catalytic subunit (GCLC) delays cataract formation.Science advances · 2024Article
- Transcriptome exploration of ferroptosis-related genes in TGFβ- induced lens epithelial to mesenchymal transition during posterior capsular opacification development.BMC genomics · 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
- Glutathione: A Key Regulator of Extracellular Matrix and Cell Death in Intervertebral Disc Degeneration.Mediators of inflammation · 2024Review
- Clinical Translation of Long-Acting Drug Delivery Systems for Posterior Capsule Opacification Prophylaxis.Pharmaceutics · 2023Review
- Role of Oxidative Stress in Ocular Diseases: A Balancing Act.Metabolites · 2023Review
- Oxidative stress-induced temporal activation of ERK1/2 phosphorylates coreceptor of Wnt/β-catenin for myofibroblast formation in human lens epithelial cells.Molecular vision · 2023Article
- A tamoxifen-inducible Cre knock-in mouse for lens-specific gene manipulation.Experimental eye research · 2023Article
- Augmented cellular uptake and homologous targeting of exosome-based drug loaded IOL for posterior capsular opacification prevention and biosafety improvement.Bioactive materials · 2022Article
- Article
- Toll-like receptor 3 gene regulates cataract-related mechanisms via the Jagged-1/Notch signaling pathway.Bioengineered · 2022Article
- MYPT1/PP1-Mediated EZH2 Dephosphorylation at S21 Promotes Epithelial-Mesenchymal Transition in Fibrosis through Control of Multiple Families of Genes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
The epithelial-mesenchymal transition (EMT) process plays a pivotal role in the pathogenesis of posterior capsular opacification because of remnant lens epithelial cell proliferation, migration, and transformation after cataract surgery. The latter, we hypothesize, may result in posterior capsule wrinkling and opacification because of a profound change in the lens growth environment via a 1000-fold reduction of extracellular glutathione (GSH) levels. To test this hypothesis, we investigated the EMT process in cell culture and GSH biosynthesis deficiency mouse models. Our data indicate a dramatic increase of pro-EMT markers, such as type I collagen, α-smooth muscle actin, vimentin, and fibronectin, under conditions of lens GSH depletion. Further study suggests that decreased GSH triggers the Wnt/β-catenin signal transduction pathway, independent of transforming growth factor-β. Equally important, the antioxidants N-acetyl cysteine and GSH ethyl ester could significantly attenuate the EMT signaling stimulated by decreased GSH levels. These findings were further confirmed by mock cataract surgery in both gamma glutamyl-cysteine ligase, catalytic subunit, and gamma glutamyl-cysteine ligase, modifier subunit, knockout mouse models. Remarkably, increased EMT marker expression, β-catenin activation, and translocation into the nucleus were found in both knockout mice compared with the wild type, and such increased expression could be significantly attenuated by N-acetyl cysteine or GSH ethyl ester treatment. This study, for the first time we believe, links oxidative stress to lens fibrosis and posterior capsular opacification formation via EMT-mediated mechanisms.
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