An update on advanced glycation endproducts and atherosclerosis


  • Serena Del Turco,

    1. Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy
    Search for more papers by this author
  • Giuseppina Basta

    Corresponding author
    1. Institute of Clinical Physiology, National Research Council (CNR), Pisa, Italy
    • CNR, Institute of Clinical Physiology, San Cataldo Research Area, Via Moruzzi, 1, 56124 Pisa, Italy
    Search for more papers by this author
    • Tel.: +0039-050-315 2216; Fax: +0039-050-315 2166


Advanced glycation endproducts (AGEs) are a group of modified molecular species formed by nonenzymatic reactions between the aldehydic group of reducing sugars with proteins, lipids, or nucleic acids. Formation and accumulation of AGEs are related to the aging process and are accelerated in diabetes. AGEs are generated in hyperglycemia, but their production also occurs in settings characterized by oxidative stress and inflammation. These species promote vascular damage and acceleration of atherosclerotic plaque progression mainly through two mechanisms: directly, altering the functional properties of vessel wall extracellular matrix molecules, or indirectly, through activation of cell receptor-dependent signaling. Interaction between AGEs and the key receptor for AGEs (RAGE), a transmembrane signaling receptor which is present in all cells relevant to atherosclerosis, alters cellular function, promotes gene expression, and enhances the release of proinflammatory molecules. The importance of the AGE-RAGE interaction and downstream pathways, leading to vessel wall injury and plaque development, has been amply established in animal studies. Moreover, the deleterious link of AGEs with diabetic vascular complications has been suggested in many human studies. Blocking the vicious cycle of AGE-RAGE axis signaling may be essential in controlling and preventing cardiovascular complications. In this article, we review the pathogenetic role of AGEs in the development, progression and instability of atherosclerosis, and the potential targets of this biological system for the prevention and treatment of cardiovascular disease. © 2012 International Union of Biochemistry and Molecular Biology, Inc.