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. Epub 2019 Jan 3.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Coronary Artery Disease / etiology*
  • Coronary Artery Disease / genetics
  • Coronary Artery Disease / metabolism
  • Coronary Artery Disease / therapy
  • Glycation End Products, Advanced / metabolism
  • Glycation End Products, Advanced / physiology*
  • Humans
  • Molecular Targeted Therapy / methods
  • Myocytes, Smooth Muscle / metabolism
  • Oxidative Stress / physiology
  • Receptor for Advanced Glycation End Products / metabolism
  • Receptor for Advanced Glycation End Products / physiology*
  • Signal Transduction / physiology


  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products