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Impact of advanced glycation end products (AGEs) signaling in coronary artery disease
Open accessAbstract
Coronary artery disease remains the leading cause of mortality in adult diabetic population with however, a high predominance also in non-diabetic subjects. In search of common molecular mechanisms and metabolic by-products with potential pathogenic role, increased advanced glycation end products (AGEs) present a critical biomarker for CAD development in both cases. Interaction of AGEs with their transmembrane cell receptor, RAGE in endothelial and smooth muscle cells as well as in platelets, activates intracellular signaling that leads to endothelial injury, modulation of vascular smooth muscle cell function and altered platelet activity. Furthermore, tissue accumulation of AGEs affects current treatment approaches being involved in stent restenosis. The present review provides an update of AGE-induced molecular mechanisms involved in CAD pathophysiology while it discusses emerging therapeutic interventions targeting AGE reduction and AGE-RAGE signaling with beneficial clinical outcome.
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“AGEs can stimulate cardiovascular complications in the presence or absence of hyperglycemia58.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [58]
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Mehta, J. K., Banerjee, M., Shah, P. H., Kaur, G., & Buttar, H. S. (2023) · Advances in biochemistry in health and disease · doi:10.1007/978-3-031-14952-8_14 · Cited by 2
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Fedai, H., & Taşcanov, M. B. (2022) · Combinatorial Chemistry & High Throughput Screening · doi:10.2174/1386207326666221026151525 · Cited by 1
AGE-RAGE Pathway as a Potential Therapeutic Target
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Metadata
- Authors
- Kosmopoulos, M., Drekolias, D., Zavras, P. D., Piperi, C., & Papavassiliou, A. G.
- Affiliations
- National and Kapodistrian University of Athens (GR)
- Corresponding author
- Piperi, Christina
- Papavassiliou, Athanasios G.
- ORCID
- Venue
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
- Publisher
- Elsevier BV
- Published
- 2019-03
- Volume
- 1865
- Issue
- 3
- Pages
- 611-619
- ISSN
- 0925-4439 (ISSN-L)
- OpenAlex
- W2907553212
- Cited by
- 136
- References
- 103
- Citations by year
- 2026: 15 · 2025: 22 · 2024: 20 · 2023: 27 · 2022: 21 · 2021: 14 · 2020: 11 · 2019: 5
- FWCI
- 1.66
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
- PubMed (publishedVersion)
- 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 › Nephrology › Chronic Kidney Disease and Diabetes
- Keywords
- advanced glycation end products, RAGE, receptor for advanced glycation end products, coronary artery disease, AGE-RAGE signaling pathway, endothelial injury, vascular smooth muscle cells, platelet activation, in-stent restenosis, diabetic cardiovascular disease, biomarkers
- MeSH terms
- Receptor for Advanced Glycation End Products, Animals, Coronary Artery Disease, Humans, Signal Transduction, Glycation End Products, Advanced, Oxidative Stress, Myocytes, Smooth Muscle, Molecular Targeted Therapy
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