ArticleMolecular medicine (Cambridge, Mass.)2023
AGEs promote atherosclerosis by increasing LDL transcytosis across endothelial cells via RAGE/NF-κB/Caveolin-1 pathway.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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35 citing papers in PubMed, 46 citations in OpenAlex.
- Post‑translational modifications in atherosclerosis: Roles, mechanisms and therapeutic potential (Review).International journal of molecular medicine · 2026Review
- Trained immunity: New insights into pathogenesis and therapeutic targets in diabetes and diabetic complications.Genes & diseases · 2026Review
- Targeting the AGE-RAGE/NF-κB Pathway: An Integrative Study Decoding the Anti-Colitis Effect of Five-Flavor Sophora Flavescens Enteric-Coated Capsule.Biomedicines · 2026Article
- Histamine in Diabetic Cardiovascular Complications.Reviews in cardiovascular medicine · 2026Review
- Article
- Cell-Free DNA-Based Theranostics for Inflammatory Disorders.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- The AGE-RAGE Pathway in Endometriosis: A Focused Mechanistic Review and Structured Evidence Map.International journal of molecular sciences · 2026Review
- The Central Role of Lipid Metabolism Disorders in Diabetes Mellitus: Mechanisms, Clinical Manifestations, and Emerging Therapeutic Strategies.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- PANoptosis in diabetic retinopathy: immunological insights into mechanisms and translational therapies.Frontiers in immunology · 2026Review
- Hemoglobin glycation index and prognosis after successful chronic total occlusion percutaneous coronary intervention: a retrospective cohort study.Frontiers in endocrinology · 2026Article
- Paeonol Inhibits the MAPK Signaling Pathway by Targeting SIRT1 in AGE-Induced HUVECs Injury.Combinatorial chemistry & high throughput screening · 2026Article
- Management of dyslipidaemia in patients with comorbidities: facing the challenge: type 2 diabetes mellitus.European heart journal. Cardiovascular pharmacotherapy · 2025Review
- Systematically Revealing Quantitative Multi-Target Integrative Effects of Plants With Artificial Intelligence Method.Plant biotechnology journal · 2025Article
- Progress in the study of the role of C5a-induced tubular cell senescence in the progression of diabetic kidney disease.Annals of medicine · 2025Review
- Advanced glycation end products (AGEs) and their role in diabetes mellitus and related complications: mechanisms and therapeutic insights.Glycoconjugate journal · 2025Review
- NFĸB and its inhibitors in preeclampsia: mechanisms and potential interventions.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- A Metabolic Signature Specific to the Patients with Type 2 Diabetes and its Association with the Pathogenesis of Diabetic-Foot Syndrome.Journal of cardiovascular translational research · 2025Article
- The Role of Advanced Glycation End-Products in the Pathophysiology and Pharmacotherapy of Cardiovascular Disease.International journal of molecular sciences · 2025Review
- PPP2CB aggravates atherosclerosis-related dyslipidemia via LOX-1/MAPK/ERK signaling pathway.Lipids in health and disease · 2025Article
- Dihydromyricetin May Attenuate Skin Aging as a RAGE Inhibitor.Nutrients · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo elucidate the mechanism whereby advanced glycation end products (AGEs) accelerate atherosclerosis (AS) and to explore novel therapeutic strategies for atherosclerotic cardiovascular disease. METHODS AND
resultsThe effect of AGEs on low-density lipoprotein (LDL) transcytosis across endothelial cells (ECs) was assessed using an in vitro model of LDL transcytosis. We observed that AGEs activated the receptor for advanced glycation end products (RAGE) on the surface of ECs and consequently upregulated Caveolin-1, which in turn increased caveolae-mediated LDL transcytosis and accelerated AS progression. Our molecular assessment revealed that AGEs activate the RAGE-NF-κB signaling, which then recruits the NF-κB subunit p65 to the RAGE promoter and consequently enhances RAGE transcription, thereby forming a positive feedback loop between the NF-κB signaling and RAGE expression. Increased NF-κB signaling ultimately upregulated Caveolin-1, promoting LDL transcytosis, and inhibition of RAGE suppressed AGE-induced LDL transcytosis. In ApoE
conclusionAGEs accelerate the development of diabetes-related AS by increasing the LDL transcytosis in ECs through the activation of the RAGE/NF-κB/Caveolin-1 axis, which may be targeted to prevent or treat diabetic macrovascular complications.
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