Activation of the receptor for advanced glycation end products and consequences on health.

Autor: Wautier MP; Laboratoire de Biologie Vasculaire et Cellulaire, 6 rue Alexandre Cabanel, 75015 Paris, France., Guillausseau PJ; Université Denis Diderot Paris 7, 10 avenue de Verdun, 75010 Paris, France; APHP, Département de Médecine Interne, Hôpital Lariboisière 2 rue Ambroise Paré, 75010 Paris, France., Wautier JL; Université Denis Diderot Paris 7, 10 avenue de Verdun, 75010 Paris, France; Laboratoire de Biologie Vasculaire et Cellulaire, 6 rue Alexandre Cabanel, 75015 Paris, France. Electronic address: jltwautier@gmail.com.
Jazyk: angličtina
Zdroj: Diabetes & metabolic syndrome [Diabetes Metab Syndr] 2017 Oct - Dec; Vol. 11 (4), pp. 305-309. Date of Electronic Publication: 2016 Sep 04.
DOI: 10.1016/j.dsx.2016.09.009
Abstrakt: Advanced glycation end products (AGE) resulted from a reaction between free amino group of proteins and carbohydrates. This reaction is followed by oxidation and molecular rearrangement. Alternatively AGEs can be produced by glycolysis and oxidation. AGEs bind to a cellular receptor RAGE. RAGE engagement by ligands AGE, β-amyloid peptide, and S100 calgranulin induces a stimulation of NADPH oxidase, reactive oxygen intermediate formation, NFκB activation and gene transcription. This cascade of reaction leads to an inflammatory reaction responsible for alteration of microvessels in the retina and the kidney. Blockade of RAGE by antibodies anti-RAGE, TTP488 (azeliragon), or rRAGE prevents or limits the deleterious effect of AGEs.
(Copyright © 2016 Diabetes India. Published by Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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