The DOI matches its Crossref record; 100 of the 100 references it cites were found in a registry or an index.
The RAGE Axis: A Fundamental Mechanism Signaling Danger to the Vulnerable Vasculature
Open accessAbstract
The immunoglobulin superfamily molecule RAGE (receptor for advanced glycation end product) transduces the effects of multiple ligands, including AGEs (advanced glycation end products), advanced oxidation protein products, S100/calgranulins, high-mobility group box-1, amyloid-beta peptide, and beta-sheet fibrils. In diabetes, hyperglycemia likely stimulates the initial burst of production of ligands that interact with RAGE and activate signaling mechanisms. Consequently, increased generation of proinflammatory and prothrombotic molecules and reactive oxygen species trigger further cycles of oxidative stress via RAGE, thus setting the stage for augmented damage to diabetic tissues in the face of further insults. Many of the ligand families of RAGE have been identified in atherosclerotic plaques and in the infarcted heart. Together with increased expression of RAGE in diabetic settings, we propose that release and accumulation of RAGE ligands contribute to exaggerated cellular damage. Stopping the vicious cycle of AGE-RAGE and RAGE axis signaling in the vulnerable heart and great vessels may be essential in controlling and preventing the consequences of diabetes.
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Citations
Cites
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Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
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RAGE Mediates a Novel Proinflammatory Axis
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Self-citationThe Receptor for Advanced Glycation End Products (RAGE) Is a Cellular Binding Site for Amphoterin
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Self-citationActivation of NADPH oxidase by AGE links oxidant stress to altered gene expression via RAGE
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Ormazábal, V., Nair, S., Elfeky, O. W. M., Aguayo, C. R., Salomón, C., & Zuñiga, F. A. (2018) · Cardiovascular Diabetology · doi:10.1186/s12933-018-0762-4 · Cited by 2,432
Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I
Paneni, F., Beckman, J. A., Creager, M. A., & Cosentino, F. (2013) · European Heart Journal · doi:10.1093/eurheartj/eht149 · Cited by 1,455
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Metadata
- Authors
- Yan, S. F., Ramasamy, R., & Schmidt, A. M.
- Affiliations
- Columbia University (US)
- Venue
- Circulation Research
- Published
- 2010-03-19
- Volume
- 106
- Issue
- 5
- Pages
- 842-853
- ISSN
- 0009-7330 (ISSN-L)
- 1524-4571
- PMC
- PMC2862596
- OpenAlex
- W2118046722
- Cited by
- 381
- References
- 100
- Citations by year
- 2026: 11 · 2025: 18 · 2024: 10 · 2023: 17 · 2022: 22 · 2021: 22 · 2020: 21 · 2019: 20 · 2018: 23 · 2017: 25 · 2016: 21 · 2015: 26 · 2014: 34 · 2013: 34 · 2012: 34
- FWCI
- 3.64
- Type
- journal article
- Language
- en
- Update notices
- correction (2010-04-30)
- Open access
- bronze
- doi.org
- Locations
- Circulation Research (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P01AG026467)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Aldose Reductase and Taurine
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- receptor for advanced glycation end products, RAGE, advanced glycation end products, advanced oxidation protein products, S100/calgranulins, high mobility group box 1, amyloid-beta, β-sheet fibrils, diabetes mellitus, hyperglycemia, oxidative stress, inflammation, thrombosis, atherosclerosis, diabetic cardiomyopathy
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Blood Vessels, Cardiovascular Diseases, Diabetes Mellitus, Humans, Immunity, Innate, Ligands, Polymorphism, Genetic, Protein Processing, Post-Translational, Receptors, Immunologic, Signal Transduction, Diabetes Complications, Adaptive Immunity
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