ArticleThe Journal of biological chemistry2011
Advanced glycation end products (AGEs) induce apoptosis via a novel pathway: involvement of Ca2+ mediated by interleukin-8 protein.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 68 citations in OpenAlex.
- In Vitro Digestive-Enzyme Inhibition and Antiglycation Activity ofCurrent issues in molecular biology · 2026Article
- Advanced Glycation End Products in Disease Development and Potential Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- The Role of Advanced Glycation End Products in Saphenous Vein Graft Failure.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2025Article
- Challenges and Solutions in Advanced Management of Diabetic Foot Infections: A Review of Recent Studies.Journal of diabetes research · 2025Review
- Narrative review on nanoparticles based on current evidence: therapeutic agents for diabetic foot infection.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Antox targeting AGE/RAGE cascades to restore submandibular gland viability in rat model of type 1 diabetes.Scientific reports · 2024Article
- Article
- Intra-articular site-specific distribution of advanced glycation end products in the shoulder of patients with diabetes mellitus having rotator cuff tears.Molecular biology reports · 2023Article
- Protein Advanced Glycation End Products and Their Implications in Pancreatic Cancer.Cancer prevention research (Philadelphia, Pa.) · 2023Review
- Elicitation of Inhibitory Effects for AGE-Induced Oxidative Stress in Rotator Cuff-Derived Cells by Apocynin.Current issues in molecular biology · 2023Article
- Diabetic foot ulcer: A comprehensive review of pathophysiology and management modalities.World journal of clinical cases · 2023Review
- Beneficial Effects of a Blended Fibroin/Aloe Gel Extract Film on the Biomolecular Mechanism(s)ACS omega · 2023Article
- AGE-RAGE axis culminates into multiple pathogenic processes: a central road to neurodegeneration.Frontiers in molecular neuroscience · 2023Review
- Artemisia alleviates AGE-induced liver complications via MAPK and RAGE signaling pathways modulation: a combinatorial study.Molecular and cellular biochemistry · 2022Article
- Naturally occurring deamidated triosephosphate isomerase is a promising target for cell-selective therapy in cancer.Scientific reports · 2022Article
- Low-grade inflammation in survivors of childhood cancer and testicular cancer and its association with hypogonadism and metabolic risk factors.BMC cancer · 2022Article
- Advanced Glycation End Products Increase Salivary Gland Hypofunction in d-Galactose-Induced Aging Rats and Its Prevention by Physical Exercise.Current issues in molecular biology · 2021Article
- Article
- Impaired osteogenic differentiation and enhanced cellular receptor of advanced glycation end products sensitivity in patients with type 2 diabetes.Journal of bone and mineral metabolism · 2017Article
- Involvement of Endoplasmic Reticulum Stress, Autophagy, and Apoptosis in Advanced Glycation End Products-Induced Glomerular Mesangial Cell Injury.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Advanced glycation end products (AGEs) accumulate in diabetic patients due to high blood glucose levels and cause multiple deleterious effects. In this study, we provide evidence that the AGE increased cell death, one such deleterious effect. Methyl glyoxal-coupled human serum albumin (AGE-HSA) induced transcription factors such as NF-κB, NF-AT, and AP-1. AGE acts through its cell surface receptor, RAGE, and degranulates vesicular contents including interleukin-8 (IL-8). The number of RAGEs, as well as the amount of NF-κB activation, is low, but the cell death is higher in neuronal cells upon AGE treatment. Degranulated IL-8 acts through its receptors, IL-8Rs, and induces sequential events in cells: increase in intracellular Ca(2+), activation of calcineurin, dephosphorylation of cytoplasmic NF-AT, nuclear translocation of NF-AT, and expression of FasL. Expressed FasL increases activity of caspases and induces cell death. Although AGE increases the amount of reactive oxygen intermediate, accompanying cell death is not dependent upon reactive oxygen intermediate. AGE induces autophagy, which partially protects cells from cell death. A novel mechanism of AGE-mediated cell death in different cell types, especially in neuronal cells where it is an early event, is provided here. Thus, this study may be important in several age-related neuronal diseases where AGE-induced apoptosis is observed because of high amounts of AGE.
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