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

Marie-Paule Wautier1, Pierre-Jean Guillausseau2, Jean-Luc Wautier3

  • 1Laboratoire de Biologie Vasculaire et Cellulaire, 6 rue Alexandre Cabanel, 75015 Paris, France.

Diabetes & Metabolic Syndrome
|September 11, 2016
PubMed

Insights

Advanced glycation end products (AGEs) trigger inflammation by binding to the RAGE receptor, damaging microvessels. Blocking RAGE with therapies like azeliragon may prevent this damage.

Area of Science:

  • Biochemistry
  • Cellular Biology
  • Pathophysiology

Background:

  • Advanced glycation end products (AGEs) form from protein-carbohydrate reactions, oxidation, or glycolysis.
  • AGEs bind to the Receptor for Advanced Glycation End products (RAGE).
  • RAGE activation by ligands like AGEs initiates inflammatory pathways involving NADPH oxidase and NFκB.

Purpose of the Study:

  • To investigate the role of AGEs and RAGE in microvascular damage.
  • To evaluate the therapeutic potential of blocking RAGE to mitigate AGE-induced inflammation.

Main Methods:

  • Studied the formation and binding of AGEs to RAGE.
  • Investigated the downstream signaling cascade initiated by RAGE engagement.
  • Examined the effects of RAGE blockade using anti-RAGE antibodies, TTP488 (azeliragon), and rRAGE.

Main Results:

  • RAGE activation by AGEs stimulates NADPH oxidase, leading to reactive oxygen species.
  • This cascade results in NFκB activation and gene transcription, causing inflammation.
  • Inflammation mediated by AGE-RAGE signaling damages retinal and kidney microvessels.
  • RAGE blockade demonstrated a preventative or limiting effect on AGE-induced microvascular damage.

Conclusions:

  • The AGE-RAGE axis is a key driver of inflammatory microvascular complications.
  • Targeting RAGE offers a promising therapeutic strategy for conditions associated with AGE accumulation.
Keywords:
Cell activationDiabetes mellitusGlycationRAGE blockersReceptor for advanced glycation end products

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