The DOI matches its Crossref record; 177 of the 179 references it cites were found in a registry or an index.
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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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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In the citing paper
“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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1 retracted
Ma, H., Li, S., Xu, P., Babcock, S. A., Dolence, E. K., Brownlee, M., Li, J., & Ren, J. T. (2008) · Journal of Cellular and Molecular Medicine · doi:10.1111/j.1582-4934.2008.00547.x · Cited by 154
RetractedLópez-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013) · Cell · doi:10.1016/j.cell.2013.05.039 · Cited by 14,982
Biochemistry and molecular cell biology of diabetic complications
Brownlee, M. (2001) · Nature · doi:10.1038/414813a · Cited by 9,107 · cited 1×
“…anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript Diabetic macroangiopathy The detoxification of α-DCs, a precursor of AGE, also underlies the prevention of diabetesmediated micro and macro vascular damage that may contribute to atherosclerosis and stroke (Brownlee, 2001, 2005).”
The Pathobiology of Diabetic Complications
Brownlee, M. (2005) · Diabetes · doi:10.2337/diabetes.54.6.1615 · Cited by 5,339 · cited 3×
“…anuscript A uthor M anuscript A uthor M anuscript A uthor M anuscript Diabetic macroangiopathy The detoxification of α-DCs, a precursor of AGE, also underlies the prevention of diabetesmediated micro and macro vascular damage that may contribute to atherosclerosis and stroke (Brownlee, 2001, 2005).”
BackgroundGupta, A., & Uribarri, J. (2016) · Hormone Research in Paediatrics · doi:10.1159/000444053 · Cited by 4,023
Chronic Inflammation (Inflammaging) and Its Potential Contribution to Age-Associated Diseases
Franceschi, C., & Campisi, J. (2014) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/glu057 · Cited by 3,891
Advanced Glycation End Products and Diabetic Complications
Singh, V. P., Bali, A., Singh, N., & Jaggi, A. S. (2014) · The Korean Journal of Physiology & Pharmacology · doi:10.4196/kjpp.2014.18.1.1 · Cited by 1,518
The use of animal models in diabetes research
King, A. J. (2012) · British Journal of Pharmacology · doi:10.1111/j.1476-5381.2012.01911.x · Cited by 1,303 · cited 1×
“Vertebrate model organisms such as rodents are a natural first choice to model AGEmediated pathologies, due to the relatively close link to human disease biology and a track record as a model for studying disease pathology in diabetes (King, 2012).”
BackgroundAminoguanidine Prevents Diabetes-Induced Arterial Wall Protein Cross-Linking
Brownlee, M., Vlassara, H., Kooney, A., Ulrich, P. C., & Cerami, A. (1986) · Science · doi:10.1126/science.3487117 · Cited by 1,146
Structure Elucidation of a Senescence Cross-Link from Human Extracellular Matrix
Sell, D. R., & Monnier, V. M. (1989) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(20)88225-8 · Cited by 1,082
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2 of the 179 references couldn’t be matched to a known paper.
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From discoveries in ageing research to therapeutics for healthy ageing
Campisi, J., Kapahi, P., Lithgow, G. J., Melov, S., Newman, J. C., & Verdin, E. (2019) · Nature · doi:10.1038/s41586-019-1365-2 · Cited by 1,389
Self-citationKang, Q., & Yang, C. (2020) · Redox Biology · doi:10.1016/j.redox.2020.101799 · Cited by 1,134
“During the process, large amounts of free radicals are produced, which in turn promotes AGE formation [69].”
BackgroundAdvanced Glycation End Products and Diabetes Mellitus: Mechanisms and Perspectives
Khalid, M., Petroianu, G. A., & Adem, A. (2022) · Biomolecules · doi:10.3390/biom12040542 · Cited by 972
“Maillard reaction generates highly reactive numerous intermediate carbonyl precursors of AGEs [20,29].”
BackgroundTwarda‐Clapa, A., Olczak, A., Białkowska, A. M., & Koziołkiewicz, M. (2022) · Cells · doi:10.3390/cells11081312 · Cited by 829
Mechanisms of Oxidative Stress in Metabolic Syndrome
Masenga, S. K., Kabwe, L. S., Chakulya, M., & Kirabo, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24097898 · Cited by 816
“(3) Triose phosphates produce methylglyoxal, the main precursor of advanced glycation end products (AGEs) [63].”
Background
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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