Cited by 521Advanced Glycation End Products researchAldose Reductase and TaurineChronic Kidney Disease and Diabetes

Receptor for AGE (RAGE): Signaling mechanisms in the pathogenesis of diabetes and its complications

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Ramasamy, Ravichandran, Yan, Shi Fang, Schmidt, Ann Marie·2011·Annals of the New York Academy of Sciences

Abstract

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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Crossref · 10.1111/j.1749-6632.2011.06320.x

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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
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
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

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