Advanced glycation end-products produced systemically and by macrophages

a common contributor to inflammation and degenerative diseases

Kyunghee Byun, Yong Cheol Yoo, Myeongjoo Son, Jaesuk Lee, Goo-Bo Jeong, Young Mok Park*, Ghasem Hosseini Salekdeh, Bonghee Lee

*Corresponding author for this work

Research output: Contribution to journalReview article

62 Citations (Scopus)
114 Downloads (Pure)

Abstract

Advanced glycation end products (AGEs) and their receptor have been implicated in the progressions of many intractable diseases, such as diabetes and atherosclerosis, and are also critical for pathologic changes in chronic degenerative diseases, such as Alzheimer's disease, Parkinson's disease, and alcoholic brain damage. Recently activated macrophages were found to be a source of AGEs, and the most abundant form of AGEs, AGE-albumin excreted by macrophages has been implicated in these diseases and to act through common pathways. AGEs inhibition has been shown to prevent the pathogenesis of AGEs-related diseases in human, and therapeutic advances have resulted in several agents that prevent their adverse effects. Recently, anti-inflammatory molecules that inhibit AGEs have been shown to be good candidates for ameliorating diabetic complications as well as degenerative diseases. This review was undertaken to present, discuss, and clarify current understanding regarding AGEs formation in association with macrophages, different diseases, therapeutic and diagnostic strategy and links with RAGE inhibition.

Original languageEnglish
Pages (from-to)44-55
Number of pages12
JournalPharmacology and Therapeutics
Volume177
DOIs
Publication statusPublished - Sep 2017
Externally publishedYes

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Bibliographical note

Copyright the Author(s) 2017. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

Keywords

  • Advanced glycation end products (AGEs)
  • Receptor for AGEs (RAGE)
  • Macrophage
  • Inflammation
  • Degenerative diseases

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