Molecular strategies to prevent, inhibit, and degrade advanced glycoxidation and advanced lipoxidation end products

Free Radic Res. 2013 Aug:47 Suppl 1:93-137. doi: 10.3109/10715762.2013.792926. Epub 2013 May 7.

Abstract

The advanced glycoxidation end products (AGEs) and lipoxidation end products (ALEs) contribute to the development of diabetic complications and of other pathologies. The review discusses the possibilities of counteracting the formation and stimulating the degradation of these species by pharmaceuticals and natural compounds. The review discusses inhibitors of ALE and AGE formation, cross-link breakers, ALE/AGE elimination by enzymes and proteolytic systems, receptors for advanced glycation end products (RAGEs) and blockade of the ligand-RAGE axis.

Publication types

  • Review

MeSH terms

  • Antioxidants / metabolism*
  • Antioxidants / pharmacology
  • Cross-Linking Reagents / metabolism
  • Cross-Linking Reagents / pharmacology
  • Diabetes Complications / metabolism
  • Diabetes Mellitus / drug therapy*
  • Diabetes Mellitus / metabolism
  • Diabetes Mellitus / physiopathology
  • Glycation End Products, Advanced / antagonists & inhibitors
  • Glycation End Products, Advanced / metabolism*
  • Humans
  • Lipid Peroxidation*
  • Proteasome Endopeptidase Complex / drug effects
  • Proteasome Endopeptidase Complex / metabolism
  • Proteolysis / drug effects
  • Receptor for Advanced Glycation End Products / metabolism

Substances

  • Antioxidants
  • Cross-Linking Reagents
  • Glycation End Products, Advanced
  • Receptor for Advanced Glycation End Products
  • Proteasome Endopeptidase Complex