한빛사논문
- 조회1,240
Abstract
Kyunghee Byuna, b, 1, YongCheol Yooc, 1, Myeongjoo Sonb, Jaesuk Leea, Goo-Bo Jeongb, Young Mok Parkc, 1, Ghasem Hosseini Salekdehd, 1, Bonghee Leea, b, 1
a Center for Genomics and Proteomics, Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon 406-840, Republic of Korea
b Department of Anatomy and Cell Biology, Gachon University Graduate School of Medicine, Incheon 406-799, Republic of Korea
c Center for Cognition and Sociality, Institute for Basic Science (IBS), Daejeon 305-811, Republic of Korea
d Department of Molecular Systems Biology, Cell Science Research Center, Royan Institute for Stem Cell Biology and Technology, ACECR, Tehran, Iran
1 These authors contributed equally to this work.
*Corresponding authors
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.
논문정보
- Review Paper
- 2017년 02월 (BRIC 등록일 2017-03-02)
- 국내(교신)+국외 연구진
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