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The Role of Advanced Glycation End Products in Aging and Metabolic Diseases: Bridging Association and Causality
Open accessAbstract
Accumulation of advanced glycation end products (AGEs) on nucleotides, lipids, and peptides/proteins are an inevitable component of the aging process in all eukaryotic organisms, including humans. To date, a substantial body of evidence shows that AGEs and their functionally compromised adducts are linked to and perhaps responsible for changes seen during aging and for the development of many age-related morbidities. However, much remains to be learned about the biology of AGE formation, causal nature of these associations, and whether new interventions might be developed that will prevent or reduce the negative impact of AGEs-related damage. To facilitate achieving these latter ends, we show how invertebrate models, notably Drosophila melanogaster and Caenorhabditis elegans, can be used to explore AGE-related pathways in depth and to identify and assess drugs that will mitigate against the detrimental effects of AGE-adduct development.
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“The fundamental role of AGEs, including glycoxidation products, in human aging, but also in aging of vertebrate and invertebrate model organism has been reviewed in 2018 by Chaudhuri and colleagues [153]”
From Protein oxidation - Formation mechanisms, detection and relevance as biomarkers in human diseases (2021) · cites this paper as [153]
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“a growing body of evidence reveals that levels of glycoxidation products increase as a function of age in several tissues, dependent on the dietary intake and the presence of hyperglycemic conditions [152,153]”
From Protein oxidation - Formation mechanisms, detection and relevance as biomarkers in human diseases (2021) · cites this paper as [153]
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“together indicating the relevance of AGEs as biomarkers of aging and age-related diseases”
From Protein oxidation - Formation mechanisms, detection and relevance as biomarkers in human diseases (2021) · cites this paper as [153]
In the citing paper
“However, under pathological conditions, RAGEs can be upregulated and participate in various aging-related pathophysiologies, such as adult-onset type 2 diabetes mellitus (DM), cardiovascular disorders, myocardial infarction, chronic kidney failure, pancreatitis, cancer, Alzheimer’s disease (AD), Parkinson’s disease (PD), hepatic fibrosis, and alcohol-mediated tissue injury37,38.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [37]
In the citing paper
“Generally, RAGEs are expressed widely in various cells, such as endothelial cells, macrophages/monocytes, neutrophils, lymphocytes, microglia, astrocytes, and neurons, and organs, such as the brain, heart, lung, kidney, and liver36,37.”
From Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury (2021) · cites this paper as [37]
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“AGEs include various isomers and heterogeneous groups of compounds, example the MGO-derived AGEs (AGE4), which contain N ε -carboxyethyl-lysine (CEL), methylglyoxal lysine dimer (MOLD), methylgly-oxal hydroimidazolone (MG-H1), and other molecules [3].”
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“These compounds are associated with protein cross-linking, oxidative stress, and chronic diseases such as diabetes and cardiovascular disorders (Chaudhuri et al., 2018; Xu et al., 2018).”
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“AGEs are recognized as a molecular mechanism underlying aging and chronic diseases, including Alzheimer's disease, coronary artery disease, cancer, and diabetes, through inflammation and oxidative stress [13].”
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“AGEs accumulate in particular in the case of several pathologies such as cardiovascular or neurodegenerative diseases (see e.g. Poulsen et al. 2013; Chaudhuri et al. 2018; Twarda-clapa et al. 2022; Khalid, et al. 2022).”
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Metadata
- Authors
- Chaudhuri, J., Bains, Y., Guha, S., Kahn, A., Hall, D., Bose, N., Gugliucci, A., & Kapahi, P.
- Affiliations
- Buck Institute for Research on Aging (US)
- Touro University California (US)
- Corresponding author
- Chaudhuri, Jyotiska
- Gugliucci, Alejandro
- Kapahi, Pankaj
- Venue
- Cell Metabolism
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 28
- Issue
- 3
- Pages
- 337-352
- ISSN
- 1550-4131 (ISSN-L)
- PMC
- PMC6355252
- OpenAlex
- W2892213316
- Cited by
- 669
- References
- 179
- Citations by year
- 2026: 70 · 2025: 118 · 2024: 91 · 2023: 107 · 2022: 83 · 2021: 116 · 2020: 48 · 2019: 34 · 2018: 1
- FWCI
- 6.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Touro Scholar (Touro College) (submittedVersion)
- Funders
- American Federation for Aging Research
- Larry L. Hillblom Foundation
- impact circle award
- NIH (R21 AG053066, RO1 AG045835, RO1 5RO1HL113887)
- Touro University California
- NIH/NIA (T32 AG000266)
- Hillblom Foundation Postdoctoral Fellowship
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Agricultural and Biological Sciences › Food Science › Potato Plant Research
- Keywords
- advanced glycation end products, aging, metabolic disorders, AGE formation, age-related diseases, Drosophila melanogaster, Caenorhabditis elegans, invertebrate models, drug screening
- MeSH terms
- Aging, Animals, Drosophila melanogaster, Humans, Metabolic Diseases, Yeasts, Signal Transduction, Glycation End Products, Advanced, Caenorhabditis elegans, Oxidative Stress, Neurodegenerative Diseases, Models, Animal, Mice, Rats
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