Advanced glycation end products in diabetes-associated atherosclerosis and renal disease: Interventional studies

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Abstract

There is increasing evidence that advanced glycation end products (AGEs) and their interactions with various receptors (in particular, the receptor RAGE) play a pivotal role in the development and progression of diabetic macro- and microvascular complications. Several approaches have been used to inhibit tissue accumulation of AGEs in diabetes, including inhibitors of AGE formation such as aminoguanidine, ALT 946, and pyridoxamine-or putative cross-link breakers such as ALT 711. Alternative interventions have also included the administration of a soluble receptor for RAGE, sRAGE, thus capturing circulating AGEs and preventing them from binding to the cell-bound full-length receptor RAGE, thereby inhibiting the proinflammatory and profibrotic response following AGE-RAGE binding. In this review we summarize the evidence for such antiglycation therapies in retarding or delaying the development and progression of diabetes-associated atherosclerosis and renal disease while focusing on interventional strategies inhibiting AGE accumulation. In summary, all approaches have been shown to confer some degree of antiatherosclerotic and renoprotective effects, albeit to different degrees and by different mechanisms.

Original languageEnglish
Pages (from-to)759-766
Number of pages8
JournalAnnals of the New York Academy of Sciences
Volume1043
DOIs
Publication statusPublished - 1 Jan 2005
Externally publishedYes

Keywords

  • Advanced glycation end products (AGEs)
  • Aminoguanidine
  • Atherosclerosis
  • Cross-link breaker
  • Diabetes
  • Nephropathy
  • Pyridoxamine
  • RAGE
  • Soluble RAGE

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