Cited by 357Advanced Glycation End Products researchPotato Plant ResearchChronic Kidney Disease and Diabetes

Advanced glycation end-products produced systemically and by macrophages: A common contributor to inflammation and degenerative diseases

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Byun, Kyunghee, Yoo, YongCheol, Son, Myeongjoo, Lee, Jaesuk, Jeong, Goo-Bo, Park, Young Mok, Salekdeh, Ghasem Hosseini, Lee, Bonghee·2017·Pharmacology & Therapeutics

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.

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Crossref · 10.1016/j.pharmthera.2017.02.030

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  • AGEs contribute to the development and progression of various aging-related pathological conditions, including diabetes, cardiovascular complications, gut microbiome-associated illnesses, liver or neurodegenerative diseases, and cancer.

    “Recent studies in basic and translational research have revealed the contributing roles of AGEs in the development and progression of various aging-related pathological conditions, such as diabetes, cardiovascular complications, gut microbiome-associated illnesses, liver or neurodegenerative diseases, and cancer.”
  • Endogenous AGEs are produced and slowly accumulated within the body during normal aging and under oxidative stress, inflammatory, and hyperglycemic conditions often observed in diabetes and other metabolic syndromes.

    “Endogenous AGEs represent adducts that are produced and slowly accumulated within the body during the normal aging process and under the oxidative stress, inflammatory, and hyperglycemic (high blood sugar) conditions often observed in diabetes and other metabolic syndromes1,4,12,13.”
  • Factors promoting AGE formation include excessive and/or prolonged alcohol consumption, cigarette smoking, high fat/caloric diets and/or extensively processed food, renal status, homeostatic imbalance, inflammation, hyperglycemia, and oxidative stress.

    “These factors include excessive and/or prolonged alcohol consumption, cigarette smoking, the intake of high fat/caloric diets and/or extensively processed food, renal status, homeostatic imbalance, inflammation, hyperglycemia, and oxidative stress2–4.”
  • Elevated oxidative stress can stimulate AGE accumulation, while AGE activation can increase oxidative stress, creating a synergistic feed-forward loop.

    “Additionally, elevated oxidative stress can act as a catalyst to stimulate AGE accumulation, while activation of AGEs can increase oxidative stress, creating a synergistic feed-forward loop to accelerate pathophysiological conditions2–4.”
  • The amounts of AGEs in exogenous sources are usually much higher than those of endogenously produced AGEs.

    “The amounts of AGEs in exogenous sources are usually much higher than those of endogenously produced AGEs2–4,24.”

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Research works printed but not linked: 1

  1. Ritchie, R. F., Palomaki, G. E., Neveux, L. M., Navolotskaia, O., Ledue, T. B., & Craig, W. Y. (1999). Reference distributions for the negative acute-phase serum proteins, albu- min, transferrin and transthyretin: A practical, simple and clinically relevant ap- proach in a large cohort. Journal of Clinical Laboratory Analysis 13, 273-279.

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Authors
Byun, K., Yoo, Y., Son, M., Lee, J., Jeong, G.-B., Park, Y. M., Salekdeh, G. H., & Lee, B.
Affiliations
  • Gachon University (KR)
  • Institute for Basic Science (KR)
  • Royan Institute (IR)
Corresponding author
  • Park, Young Mok
  • Salekdeh, Ghasem Hosseini
Venue
Pharmacology & Therapeutics
Publisher
Elsevier BV
Published
2017-09
Volume
177
Pages
44-55
ISSN
0163-7258 (ISSN-L)
OpenAlex
W2587891766
Cited by
357
References
193
Citations by year
2026: 27 · 2025: 40 · 2024: 47 · 2023: 43 · 2022: 40 · 2021: 57 · 2020: 37 · 2019: 32 · 2018: 24 · 2017: 10
FWCI
3.68
Type
journal article
Language
en
Open access
Locations
  • Pharmacology & Therapeutics (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • Ministry of Health & Welfare, Republic of Korea (HI13C2098)
  • National Research Foundation of Korea (2015R1A2A2A01005212)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
  • Life Sciences › Agricultural and Biological Sciences › Food Science › Potato Plant Research
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Keywords
advanced glycation end products, RAGE, macrophages, inflammation, degenerative diseases, diabetes complications, atherosclerosis, Alzheimer's disease, Parkinson's disease, alcoholic brain damage, RAGE inhibition, AGE formation
MeSH terms
Receptor for Advanced Glycation End Products, Humans, Inflammation, Macrophages, Glycation End Products, Advanced, Neurodegenerative Diseases

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