2. Academic Validation
  3. Impact of advanced glycation end products (AGEs) signaling in coronary artery disease

Impact of advanced glycation end products (AGEs) signaling in coronary artery disease

  • Biochim Biophys Acta Mol Basis Dis. 2019 Mar 1;1865(3):611-619. doi: 10.1016/j.bbadis.2019.01.006.
Marinos Kosmopoulos 1,  Dimitrios Drekolias 1,  Phaedon D Zavras 1,  Christina Piperi 2,  Athanasios G Papavassiliou 3
Affiliations

Affiliations

  • 1 Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece.
  • 2 Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece. Electronic address: [email protected].
  • 3 Department of Biological Chemistry, Medical School, National and Kapodistrian University of Athens, 11527 Athens, Greece. Electronic address: [email protected].
PMID: 30611860 DOI: 10.1016/j.bbadis.2019.01.006
Abstract

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.

Keywords

Advanced glycation end products (AGEs); Coronary artery disease; Endothelium; Platelets; RAGE; Stent restenosis.

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