Journal
PHARMACOLOGY & THERAPEUTICS
Volume 177, Issue -, Pages 44-55Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2017.02.030
Keywords
Advanced glycation end products (AGES); Receptor for AGES (RAGE); Macrophage; Inflammation; Degenerative diseases
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Funding
- Korean Health Industry Development Institute (KHIDI) - Ministry of Health & Welfare, Republic of Korea [HI13C2098]
- National Research Foundation of Korea [2015R1A2A2A01005212]
- Korea Health Promotion Institute [HI13C2098020017] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- Ministry of Science & ICT (MSIT), Republic of Korea [IBS-R001-D1-2017-A00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2015R1A2A2A01005212] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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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. (C)2017 The Author(s). Published by Elsevier Inc.
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