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Impact of Advanced Glycation End Products on Endothelial Function and Their Potential Link to Atherosclerosis

E. Álvarez,B. Paradela-Dobarro,M. González-Peteiro,J. González-Juanatey

Published 2018 in Endothelial Dysfunction - Old Concepts and New Challenges

ABSTRACT

The role of advanced glycation end products (AGEs) in cardiovascular diseases is a matter of interest in the last years and the strong association between the action of AGEs on their receptor (RAGE) and atherosclerosis has attracted increased attention. The aim of this chapter is to review the results of our laboratory and others on the molecular mechanisms triggered by AGEs in the endothelium that could participate in the ath- erosclerotic process. These mechanisms and molecular pathways could be the source of new therapeutic targets against atherosclerosis or vascular disease. Oxidative stress in endothelium induced by AGEs triggers molecular signaling pathways that produce an inflammatory response or even endothelial dysfunction. Adhesion molecules expression at the membranes of endothelial cells as a consequence of this response or induced by other mechanisms involving AGEs mediates the adhesion of leukocytes to endothelium. This adhesion is a key step in the atherogenesis process and the possible involvement of AGE-RAGE axis in this process should be considered as a potential therapeutic tar - get. Finally, potential pharmacological modulation of AGE-RAGE axis activity at the endothelium is suggested, but the specific pharmacological tools available nowadays are missing; respectively, drugs used for the treatment of cardiovascular and metabolic dis eases could be helpful for AGE-RAGE axis modulation, thus also affecting endothelial (dys)function.

PUBLICATION RECORD

  • Publication year

    2018

  • Venue

    Endothelial Dysfunction - Old Concepts and New Challenges

  • Publication date

    2018-10-24

  • Fields of study

    Medicine, Chemistry, Environmental Science

  • Identifiers
    DOI 10.5772/INTECHOPEN.73025
  • External record

    Open on Semantic Scholar

  • Source metadata

    Semantic Scholar

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