Cited by 173Advanced Glycation End Products researchNitric Oxide and Endothelin EffectsCardiovascular Health and Disease Prevention

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The AGE-RAGE Axis: Implications for Age-Associated Arterial Diseases

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Senatus, Laura M., Schmidt, Ann Marie·2017·Frontiers in Genetics

DOI 10.3389/fgene.2017.00187PMC PMC5723304

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Abstract

The process of advanced glycation leads to the generation and accumulation of an heterogeneous class of molecules called advanced glycation endproducts, or AGEs. AGEs are produced to accelerated degrees in disorders such as diabetes, renal failure, inflammation, neurodegeneration and in aging. Further, AGEs are present in foods and in tobacco products. Hence, through both endogenous production and exogenous consumption, AGEs perturb vascular homeostasis by a number of means; in the first case, AGEs can cause cross-linking of long-lived molecules in the basement membranes such as collagens, thereby leading to “vascular stiffening” and processes that lead to hyperpermeability and loss of structural integrity. Second, AGEs interaction with their major cell surface signal transduction receptor for AGE or RAGE sets off a cascade of events leading to modulation of gene expression and loss of vascular and tissue homeostasis, processes that contribute to cardiovascular disease. In addition, it has been shown that an enzyme, which plays key roles in the detoxification of pre-AGE species, glyoxalase 1 (GLO1), is reduced in aged and diabetic tissues. In the diabetic kidney devoid of Ager (gene encoding RAGE), higher levels of Glo1 mRNA and GLO1 protein and activity were observed, suggesting that in conditions of high AGE accumulation, natural defenses may be mitigated, at least in part through RAGE. AGEs are a marker of arterial aging and may be detected by both biochemical means, as well as measurement of “skin autofluorescence.” In this review, we will detail the pathobiology of the AGE-RAGE axis and the consequences of its activation in the vasculature and conclude with potential avenues for therapeutic interruption of the AGE-RAGE ligand-RAGE pathways as means to forestall the deleterious consequences of AGE accumulation and signaling via RAGE.

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Authors: Senatus, L. M., & Schmidt, A. M.
Affiliations: New York University (US)
Corresponding author: Schmidt, Ann Marie
ORCID: Senatus, Laura M.
Schmidt, Ann Marie
Venue: Frontiers in Genetics
Publisher: Frontiers Media SA
Published: 2017-12-05
Volume: 8
Pages: 187-187
ISSN: 1664-8021 (ISSN-L)
DOI: 10.3389/fgene.2017.00187
PMC: PMC5723304
OpenAlex: W2774984051
Cited by: 167
References: 96
Citations by year: 2026: 18 · 2025: 15 · 2024: 17 · 2023: 18 · 2022: 29 · 2021: 23 · 2020: 19 · 2019: 17 · 2018: 10
FWCI: 1.64
Type: journal article
Language: en
Open access: gold
doi.org
Licence: cc-by
Locations: Frontiers in Genetics (publishedVersion, cc-by)
Europe PMC (PubMed Central) (publishedVersion, cc-by)
PubMed Central (publishedVersion, cc-by)
PubMed (publishedVersion)
DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders: U.S. Public Health Service
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
Keywords: advanced glycation end products, AGE-RAGE axis, receptor for advanced glycation end products, vascular aging, arterial aging, arterial stiffness, glyoxalase I, diabetes mellitus, diabetic kidney, skin autofluorescence, AGE accumulation, cardiovascular disease, vascular homeostasis

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The AGE-RAGE Axis: Implications for Age-Associated Arterial Diseases

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