ArticleAmerican journal of translational research2016
Advanced glycation endproducts induce apoptosis of endothelial progenitor cells by activating receptor RAGE and NADPH oxidase/JNK signaling axis.
Article in American journal of translational research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 59 citations in OpenAlex.
- The AGE-RAGE-DIAPH1 Axis in Type 2 Diabetes and Metabolic Dysfunction: From Carbonyl Stress to Diabetic Myocardial and Neuronal Injury.International journal of molecular sciences · 2026Review
- The Glycemia Risk Index (GRI) as a Biomarker for Subclinical Endothelial Dysfunction in Type 1 Diabetes: A Cross-Sectional Study.International journal of molecular sciences · 2025Article
- Investigating the Inhibitory Effects of Paliperidone on RAGEs: Docking, DFT, MD Simulations, MMPBSA, MTT, Apoptosis, and Immunoblotting Studies.International journal of molecular sciences · 2025Article
- Targeting the AGEs-RAGE axis: pathogenic mechanisms and therapeutic interventions in diabetic wound healing.Frontiers in medicine · 2025Review
- Endothelial progenitor cells as biomarkers of diabetes-related cardiovascular complications.Stem cell research & therapy · 2023Review
- Hypomagnesemia and Cardiovascular Risk in Type 2 Diabetes.Endocrine reviews · 2023Article
- Mechanism of the antidiabetic action ofFrontiers in nutrition · 2023Review
- Advances in the study of the molecular biological mechanisms of radiation-induced brain injury.American journal of cancer research · 2023Review
- Selected Plant-Derived Polyphenols as Potential Therapeutic Agents for Peripheral Artery Disease: Molecular Mechanisms, Efficacy and Safety.Molecules (Basel, Switzerland) · 2022Review
- Role of Oxidative Stress in Diabetic Cardiomyopathy.Antioxidants (Basel, Switzerland) · 2022Review
- AGE/Non-AGE Glycation: An Important Event in Rheumatoid Arthritis Pathophysiology.Inflammation · 2022Review
- Exosomes: Potential Player in Endothelial Dysfunction in Cardiovascular Disease.Cardiovascular toxicology · 2022Review
- New insights into the role of melatonin in diabetic cardiomyopathy.Pharmacology research & perspectives · 2022Review
- The Correlation Between MicroRNAs and Diabetic Retinopathy.Frontiers in immunology · 2022Review
- CYT387, a JAK-Specific Inhibitor Impedes Osteoclast Activity and Oophorectomy-Induced OsteoporosisFrontiers in pharmacology · 2022Article
- Cross-Talking Pathways of Forkhead Box O1 (FOXO1) Are Involved in the Pathogenesis of Alzheimer's Disease and Huntington's Disease.Oxidative medicine and cellular longevity · 2022Article
- Diabetic Cardiomyopathy: Pathophysiology and Novel Therapies.The Brown journal of hospital medicine · 2022Review
- A Catecholaldehyde Metabolite of Norepinephrine Induces Myofibroblast Activation and Toxicity via the Receptor for Advanced Glycation Endproducts: Mitigating Role of l-Carnosine.Chemical research in toxicology · 2021Article
- Methylglyoxal-Derived Advanced Glycation End Product (AGE4)-Induced Apoptosis Leads to Mitochondrial Dysfunction and Endoplasmic Reticulum Stress through the RAGE/JNK Pathway in Kidney Cells.International journal of molecular sciences · 2021Article
- Can Metformin Exert as an Active Drug on Endothelial Dysfunction in Diabetic Subjects?Biomedicines · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Elevated levels of advanced glycation endproducts (AGEs) is an important risk factor for atherosclerosis. Dysfunction of endothelial progenitor cells (EPCs), which is essential for re-endothelialization and neovascularization, is a hallmark of atherosclerosis. However, it remains unclear whether and how AGEs acts on EPCs to promote pathogenesis of atherosclerosis. In this study, EPCs were exposed to different concentrations of AGEs. The expression of NADPH and Rac1 was measured to investigate the involvement of NADPH oxidase pathway. ROS was examined to indicate the level of oxidative stress in EPCs. Total JNK and p-JNK were determined by Western blotting. Cell apoptosis was evaluated by both TUNEL staining and flow cytometry. Cell proliferation was measured by (3)H thymidine uptake. The results showed that treatment of EPCs with AGEs increased the levels of ROS in EPCs. Mechanistically, AGEs increased the activity of NADPH oxidase and the expression of Rac1, a major component of NADPH. Importantly, treatment of EPCs with AGEs activated the JNK signaling pathway, which was closely associated with cell apoptosis and inhibition of proliferation. Our results suggest that the RAGE activation by AGEs in EPCs upregulates intracellular ROS levels, which contributes to increased activity of NADPH oxidase and expression of Rac1, thus promoting cellular apoptosis and inhibiting proliferation. Mechanistically, AGEs binding to the receptor RAGE in EPCs is associated with hyperactivity of JNK signaling pathway, which is downstream of ROS. Our findings suggest that dysregulation of the AGEs/RAGE axis in EPCs may promote atherosclerosis and identify the NADPH/ROS/JNK signaling axis as a potential target for therapeutic intervention.
Indexed as
Identifiers
27347324PMC4891429W2501611248What OpenQuestion holds
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.