ArticleChemico-biological interactions2017
Influence of aldose reductase on epithelial-to-mesenchymal transition signaling in lens epithelial cells.
Article in Chemico-biological interactions, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanistic Insights into Aldose Reductase-Dependent Modulation of Hypoxia-Inducible Factor-1α in Promoting Renal Fibrosis.Cell biochemistry and biophysics · 2026Article
- Aldose reductase as a regulator of ocular pathology: Mechanisms and therapeutic potential.Histology and histopathology · 2026Review
- Assessing the therapeutic effects of DPP4 Inhibitors on TGF-β2-induced Lens Opacity.Experimental eye research · 2026Article
- Aldose Reductase Involvement in EMT: Emerging Insights and Current Proposed Molecular Mechanisms.Biology · 2025Review
- Aldose Reductase Mediated Mitophagy Promotes Epithelial-Mesenchymal Transition of Hepatocytes.Hepatic medicine : evidence and research · 2025Article
- GDF-15 Attenuates the Epithelium-Mesenchymal Transition and Alleviates TGFβ2-Induced Lens Opacity.Translational vision science & technology · 2024Article
- High incidence of sebaceous gland inflammation in aldose reductase-deficient mice.Chemico-biological interactions · 2024Article
- Aldose Reductase as a Key Target in the Prevention and Treatment of Diabetic Retinopathy: A Comprehensive Review.Biomedicines · 2024Review
- Fabrication of a 3D bioprinting model for posterior capsule opacification using GelMA and PLMA hydrogel-coated resin.Regenerative biomaterials · 2024Article
- Aldose reductase inhibition decelerates optic nerve degeneration by alleviating retinal microglia activation.Scientific reports · 2023Article
- The Role of Aldose Reductase in Beta-Amyloid-Induced Microglia Activation.International journal of molecular sciences · 2022Article
- Nanogel-Facilitated In-Situ Delivery of a Cataract Inhibitor.Biomolecules · 2021Article
- The Protective Effect of Metformin Use on Early Nd:YAG Laser Capsulotomy.Investigative ophthalmology & visual science · 2021Article
- Suppression of epithelial to mesenchymal transition markers in mouse lens by a Smad7-based recombinant protein.Chemico-biological interactions · 2021Article
- EMT signaling: potential contribution of CRISPR/Cas gene editing.Cellular and molecular life sciences : CMLS · 2020Review
- Research Progress of Drug Prophylaxis for Lens Capsule Opacification after Cataract Surgery.Journal of ophthalmology · 2020Review
- 2',3'-Cyclic-nucleotide 3'-phosphodiesterase contributes to epithelial-mesenchymal transition of lens epithelial cells through the notch signalling pathway.Cell proliferation · 2019Article
- Aldose reductase inhibition enhances lens regeneration in mice.Chemico-biological interactions · 2019Article
- Aldose Reductase Inhibition Prevents Development of Posterior Capsular Opacification in an In Vivo Model of Cataract Surgery.Investigative ophthalmology & visual science · 2018Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cataract is the most frequent cause of blindness worldwide and is treated by surgical removal of the opaque lens to restore the light path to the retina. While cataract surgery is a safe procedure, some patients develop a complication of the surgery involving opacification and wrinkling of the posterior lens capsule. This process, called posterior capsule opacification (PCO), requires a second clinical treatment that can in turn lead to additional complications. Prevention of PCO is a current unmet need in the vision care enterprise. The pathogenesis of PCO involves the transition of lens epithelial cells to a mesenchymal phenotype, designated epithelial-to-mesenchymal transition (EMT). Our previous studies showed that transgenic mice designed for overexpression of human aldose reductase developed lens defects reminiscent of PCO. In the current study, we evaluated the impact of aldose reductase (AR) on expression of expression of EMT markers in the lens. Primary lens epithelial cells from AR-transgenic mice showed downregulated expression of Foxe3 and Pax6 and increased expression of α-SMA, fibronectin and snail, a pattern of gene expression typical of cells undergoing EMT. A role for AR in these changes was further confirmed when we observed that they could be normalized by treatment of cells with Sorbinil, an AR inhibitor. Smad-dependent and Smad-independent pathways are known to contribute to EMT. Interestingly, AR overexpression induced ERK but not Smad-2 activation. These results suggest that elevation of AR may lead to activation of ERK signaling and thus play a role in TGF-β/Smad independent induction of EMT in lens epithelial cells.
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