ArticleScientific reports2016
AGE-RAGE signal generates a specific NF-κB RelA "barcode" that directs collagen I expression.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 48 citations in OpenAlex.
- Review
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- GLP-1 receptor agonists and next-generation metabolic hormone therapies in chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Deciphering the Multi-Target Therapeutic Mechanisms of Traditional Chinese Medicine Against Alzheimer's Disease: A Network Pharmacology Perspective.Drug design, development and therapy · 2026Review
- Ferritinophagy Is Involved in the Advanced Glycation End Products-Induced Ferroptosis of Vascular Endothelial Cells in Diabetes Mellitus.Journal of cellular and molecular medicine · 2025Article
- RAGE Is Essential for Subretinal Fibrosis in Laser-Induced Choroidal Neovascularization: Therapeutic Implications.Investigative ophthalmology & visual science · 2025Article
- Dysglycaemia is associated with the pattern of valvular calcification in micro-computed tomography analysis: an observational study in patients with severe aortic stenosis.Cardiovascular diabetology · 2025Observational
- Indoleamine 2,3-dioxygenase-galectin-3 fusion protein remodels inflammatory and fibrotic programs, ameliorating imiquimod-induced psoriasis.npj biomedical innovations · 2025Article
- Advance Glycation End Products Inhibition byFood science & nutrition · 2024Article
- Association Between Advanced Glycation End Products and Sarcopenia: The Mediating Role of Osteoporosis.The Journal of clinical endocrinology and metabolism · 2024Article
- Review
- Post-translational modifications of p65: state of the art.Frontiers in cell and developmental biology · 2024Review
- Anhydrous microwave synthesis as efficient method for obtaining model advanced glycation end-products.Frontiers in molecular biosciences · 2024Article
- Childhood obesity, metabolic syndrome, and oxidative stress: microRNAs go on stage.Reviews in endocrine & metabolic disorders · 2023Review
- Current challenges in the treatment of cardiac fibrosis: Recent insights into the sex-specific differences of glucose-lowering therapies on the diabetic heart: IUPHAR Review 33.British journal of pharmacology · 2023Review
- Antioxidant and Anti-Inflammatory Mechanisms of Lipophilic Fractions fromFoods (Basel, Switzerland) · 2023Article
- Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.Endocrine reviews · 2023Review
- Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023Review
- Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections.International journal of molecular sciences · 2023Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Advanced glycation end products (AGEs) are sugar-modified biomolecules that accumulate in the body with advancing age, and are implicated in the development of multiple age-associated structural and functional abnormities and diseases. It has been well documented that AGEs signal via their receptor RAGE to activate several cellular programs including NF-κB, leading to inflammation. A large number of stimuli can activate NF-κB; yet different stimuli, or the same stimulus for NF-κB in different cellular settings, produce a very different transcriptional landscape and physiological outcome. The NF-κB barcode hypothesis posits that cellular network dynamics generate signal-specific post-translational modifications, or a "barcode" to NF-κB, and that a signature "barcode" mediates a specific gene expression pattern. In the current study, we established that AGE-RAGE signaling results in NF-κB activation that directs collagen Ia1 and Ia2 expression. We further demonstrated that AGE-RAGE signal induces phosphorylation of RelA at three specific residues, T254, S311, and S536. These modifications are required for transcription of collagen I genes and are a consequence of cellular network dynamics. The increase of collagen content is a hallmark of arterial aging, and our work provides a potential mechanistic link between RAGE signaling, NF-κB activation, and aging-associated arterial alterations in structure and function.
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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.