ArticleAntioxidants (Basel, Switzerland)2020
AKR1B1-Induced Epithelial-Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens.
Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 40 citations in OpenAlex.
- Article
- Aldose Reductase Involvement in EMT: Emerging Insights and Current Proposed Molecular Mechanisms.Biology · 2025Review
- Microglial metabolic reprogramming: Aucubin inhibits aldose reductase to reverse diabetic neuropathic pain.World journal of diabetes · 2025Article
- Puerarin alleviates high glucose-induced lens epithelial cell damage by activating the Nrf2 Signaling pathway to inhibit oxidative stress.Toxicology research · 2025Article
- Network pharmacology combined with molecular docking and dynamics to assess the synergism of esculetin and phloretin against acute kidney injury-diabetes comorbidity.Molecular diversity · 2025Article
- The Synergistic Effects of Polyol Pathway-Induced Oxidative and Osmotic Stress in the Aetiology of Diabetic Cataracts.International journal of molecular sciences · 2024Review
- S100A8/A9-activated IFNγCellular and molecular life sciences : CMLS · 2024Article
- Cadherin-responsive hydrogel combined with dental pulp stem cells and fibroblast growth factor 21 promotes diabetic scald repair via regulating epithelial-mesenchymal transition and necroptosis.Materials today. Bio · 2024Article
- Baicalin administration could rescue high glucose-induced craniofacial skeleton malformation by regulating neural crest development.Frontiers in pharmacology · 2024Article
- Uncovering the mechanism of resveratrol in the treatment of diabetic kidney disease based on network pharmacology, molecular docking, and experimental validation.Journal of translational medicine · 2023Article
- MicroRNA-22-3p Regulates the Apoptosis of Lens Epithelial Cells Through Targeting KLF6 in Diabetic Cataracts.Translational vision science & technology · 2023Article
- Drug repurposing for reducing the risk of cataract extraction in patients with diabetes mellitus: integration of artificial intelligence-based drug prediction and clinical corroboration.Frontiers in pharmacology · 2023Article
- Article
- Classical epithelial-mesenchymal transition (EMT) and alternative cell death process-driven blebbishield metastatic-witch (BMW) pathways to cancer metastasis.Signal transduction and targeted therapy · 2022Review
- Blocking of SGLT2 to Eliminate NADPH-Induced Oxidative Stress in Lenses of Animals with Fructose-Induced Diabetes Mellitus.International journal of molecular sciences · 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
- Paeoniflorin inhibits epithelial mesenchymal transformation and oxidative damage of lens epithelial cells in diabetic cataract via sirtuin 1 upregulation.Bioengineered · 2022Article
- Network Pharmacology-Based Strategy to Reveal the Mechanism of Cassiae Semen against Cataracts.Computational and mathematical methods in medicine · 2022Article
- 3H-1,2-Dithiole-3-Thione Protects Lens Epithelial Cells against Fructose-Induced Epithelial-Mesenchymal Transition via Activation of AMPK to Eliminate AKR1B1-Induced Oxidative Stress in Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2021Article
- microRNA-199a-5p regulates epithelial-to-mesenchymal transition in diabetic cataract by targeting SP1 gene.Molecular medicine (Cambridge, Mass.) · 2020Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
purposeCataracts are a major cause of visual acuity deterioration in diabetes mellitus (DM) in developed and developing countries. Studies have demonstrated that overproduction of AKR1B1 and receptor for advanced glycation end products (RAGE) plays a major role in the pathogenesis of diabetic cataracts, but it is unclear whether the prevalence of diabetic cataracts is related to epithelial-mesenchymal transition (EMT) in lens epithelial cells. This study aimed to analyze the role of EMT in cataract formation of DM patients.
methodsImmunofluorescence and immunohistochemistry assays were used to estimate AKR1B1, RAGE, AMPK, and EMT levels in epithelial human lens of DM or non-DM cataracts.
resultsImmunohistochemical staining demonstrated that pathologic phases and N-cadherin expression levels were significantly higher in epithelial human lens of DM (+) compared to DM (-) cataracts. Immunofluorescent staining showed that AKR1B1 and RAGE were significantly higher in epithelial human lens of DM (+) compared to DM (-) cataracts. Interestingly, acetyl superoxide dismutase 2 (AcSOD2) levels were significantly higher in DM patients' lens epithelial cells (LECs), whereas AMPKT172 phosphorylation was significantly increased in non-DM patients. This indicates that AMPKT172 might be related to superoxide reduction and diabetic cataract formation.
conclusionsOur results suggest that AKR1B1 overexpression can decrease AMPK activation, thereby increasing AcSOD2 and RAGE-induced EMT in epithelial human lens of DM cataracts. These novel findings suggest that AKR inhibitors may be candidates for the pharmacological prevention of cataracts in patients with DM.
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