ArticleGlycoconjugate journal2016
AGE-RAGE interaction in the TGFβ2-mediated epithelial to mesenchymal transition of human lens epithelial cells.
Article in Glycoconjugate journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it, 29 citations in OpenAlex.
- Potential Therapeutic Effects of Natural Plant Compounds in Kidney Disease.Molecules (Basel, Switzerland) · 2021Pooled it
- A Systems View of Posterior Capsule Opacification: TGF-β/ROS Signaling, Mitochondrial Homeostasis, and Injury/Aging Cues-Therapeutic Opportunities.Investigative ophthalmology & visual science · 2026Review
- 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
- Key post-translational modifications of crystallin: from mechanism to target exploration for cataract diagnosis and treatment.Molecular biology reports · 2025Review
- RAGE Is Essential for Subretinal Fibrosis in Laser-Induced Choroidal Neovascularization: Therapeutic Implications.Investigative ophthalmology & visual science · 2025Article
- Lens capsule advanced glycation end products induce senescence in epithelial cells: Implications for secondary cataracts.Aging cell · 2024Article
- RAGE/SNAIL1 signaling drives epithelial-mesenchymal plasticity in metastatic triple-negative breast cancer.Oncogene · 2023Article
- Mechanisms of Qing-Gan Li-Shui Formulation in Ameliorating Primary Open Angle Glaucoma: An Analysis Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Lens Fibrosis: Understanding the Dynamics of Cell Adhesion Signaling in Lens Epithelial-Mesenchymal Transition.Frontiers in cell and developmental biology · 2022Review
- Dysregulation of Receptor for Advanced Glycation End Products (RAGE) Expression as a Biomarker of Keratoconus.Disease markers · 2022Article
- Advanced glycation end products in human diabetic lens capsules.Experimental eye research · 2021Article
- Reprogramming of Mesothelial-Mesenchymal Transition in Chronic Peritoneal Diseases by Estrogen Receptor Modulation and TGF-β1 Inhibition.International journal of molecular sciences · 2020Review
- AKR1B1-Induced Epithelial-Mesenchymal Transition Mediated by RAGE-Oxidative Stress in Diabetic Cataract Lens.Antioxidants (Basel, Switzerland) · 2020Article
- Aspirin inhibits TGFβ2-induced epithelial to mesenchymal transition of lens epithelial cells: selective acetylation of K56 and K122 in histone H3.The Biochemical journal · 2020Article
- Research Progress of Drug Prophylaxis for Lens Capsule Opacification after Cataract Surgery.Journal of ophthalmology · 2020Review
- The role of HIF-1α in the TGF-β2-mediated epithelial-to-mesenchymal transition of human lens epithelial cells.Journal of cellular biochemistry · 2018Article
- Matrix-bound AGEs enhance TGFβ2-mediated mesenchymal transition of lens epithelial cells via the noncanonical pathway: implications for secondary cataract formation.The Biochemical journal · 2018Article
- REC8 inhibits EMT by downregulating EGR1 in gastric cancer cells.Oncology reports · 2018Article
- A preliminary study on the formation pathways of glycated phosphatidylethanolamine of food rich in phospholipid during the heat-processing.RSC advances · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Basement membrane (BM) proteins accumulate chemical modifications with age. One such modification is glycation, which results in the formation of advanced glycation endproducts (AGEs). In a previous study, we reported that AGEs in the human lens capsule (BM) promote the TGFβ2-mediated epithelial-to-mesenchymal transition (EMT) of lens epithelial cells, which we proposed as a mechanism for posterior capsule opacification (PCO) or secondary cataract formation. In this study, we investigated the role of a receptor for AGEs (RAGE) in the TGFβ2-mediated EMT in a human lens epithelial cell line (FHL124). RAGE was present in FHL124 cells, and its levels were unaltered in cells cultured on either native or AGE-modified BM or upon treatment with TGFβ2. RAGE overexpression significantly enhanced the TGFβ2-mediated EMT responses in cells cultured on AGE-modified BM compared with the unmodified matrix. In contrast, treatment of cells with a RAGE antibody or EN-RAGE (an endogenous ligand for RAGE) resulted in a significant reduction in the TGFβ2-mediated EMT response. This was accompanied by a reduction in TGFβ2-mediated Smad signaling and ROS generation. These results imply that the interaction of matrix AGEs with RAGE plays a role in the TGFβ2-mediated EMT of lens epithelial cells and suggest that the blockade of RAGE could be a strategy to prevent PCO and other age-associated fibrosis.
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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.