Receptor for AGE (RAGE): Signaling mechanisms in the pathogenesis of diabetes and its complications
Open accessAbstract
The receptor for advanced glycation endproducts (RAGE) was first described as a signal transduction receptor for advanced glycation endproducts (AGEs), the products of nonenzymatic glycation and oxidation of proteins and lipids that accumulate in diabetes and in inflammatory foci. The discovery that RAGE was a receptor for inflammatory S100/calgranulins and high mobility group box 1 (HMGB1) set the stage for linking RAGE to both the consequences and causes of types 1 and 2 diabetes. Recent discoveries regarding the structure of RAGE as well as novel intracellular binding partner interactions advance our understanding of the mechanisms by which RAGE evokes pathological consequences and underscore strategies by which antagonism of RAGE in the clinic may be realized. Finally, recent data tracking RAGE in the clinic suggest that levels of soluble RAGEs and polymorphisms in the gene encoding RAGE may hold promise for the identification of patients who are vulnerable to the complications of diabetes and/or are receptive to therapeutic interventions designed to prevent and reverse the damage inflicted by chronic hyperglycemia, irrespective of its etiology.
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Activation of AGE-RAGE results in increased oxidative stress, inflammation and apoptosis in ischemia-reperfusion-induced myocardial injury in diabetic rats.
“The activation of advanced glycation end products-receptor for advanced glycation end products (AGE-RAGE) results in increased oxidative stress, inflammation and apoptosis in ischemia-reperfusion (IR)-induced myocardial injury in diabetic rats (40).”
From Mangiferin: An effective therapeutic agent against several disorders (Review) (2018) · cites this paper as [40]
The animal-models section (page not provided) reports greater ischemia–reperfusion injury in diabetic mouse hearts and improvement with RAGE blockade or deletion. It also links RAGE to apoptosis and oxidative stress in isolated mouse cardiomyocytes, but does not report inflammation in the myocardial-injury experiments or findings in diabetic rats. (LLM, conf=0.88)
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- Authors
- Ramasamy, R., Yan, S. F., & Schmidt, A. M.
- Affiliations
- New York University (US)
- Corresponding author
- Schmidt, Ann Marie
- Venue
- Annals of the New York Academy of Sciences
- Publisher
- Wiley
- Published
- 2011-12
- Volume
- 1243
- Issue
- 1
- Pages
- 88-102
- ISSN
- 0077-8923 (ISSN-L)
- 1749-6632
- PMC
- PMC4501013
- OpenAlex
- W1598235393
- Cited by
- 521
- References
- 10
- Citations by year
- 2026: 30 · 2025: 41 · 2024: 47 · 2023: 45 · 2022: 38 · 2021: 37 · 2020: 38 · 2019: 28 · 2018: 29 · 2017: 30 · 2016: 25 · 2015: 35 · 2014: 32 · 2013: 41 · 2012: 22
- FWCI
- 3.62
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of the New York Academy of Sciences (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (P01AG026467)
- National Heart, Lung, and Blood Institute (P01HL060901)
- 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, diabetes pathogenesis, diabetes complications, S100/calgranulins, HMGB1, RAGE signaling, soluble RAGE, RAGE gene polymorphisms, chronic hyperglycemia, inflammation
- MeSH terms
- Receptor for Advanced Glycation End Products, Formins, Animals, Cardiovascular Diseases, Carrier Proteins, Diabetes Mellitus, Diabetic Nephropathies, Humans, Inflammation, Receptors, Immunologic, Signal Transduction, Diabetes Complications, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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