Does accumulation of advanced glycation end products contribute to the aging phenotype?
Open accessAbstract
BACKGROUND: Aging is a complex multifactorial process characterized by accumulation of deleterious changes in cells and tissues, progressive deterioration of structural integrity and physiological function across multiple organ systems, and increased risk of death. METHODS: We conducted a review of the scientific literature on the relationship of advanced glycation end products (AGEs) with aging. AGEs are a heterogeneous group of bioactive molecules that are formed by the nonenzymatic glycation of proteins, lipids, and nucleic acids. RESULTS: Humans are exposed to AGEs produced in the body, especially in individuals with abnormal glucose metabolism, and AGEs ingested in foods. AGEs cause widespread damage to tissues through upregulation of inflammation and cross-linking of collagen and other proteins. AGEs have been shown to adversely affect virtually all cells, tissues, and organ systems. Recent epidemiological studies demonstrate that elevated circulating AGEs are associated with increased risk of developing many chronic diseases that disproportionally affect older individuals. CONCLUSIONS: Based on these data, we propose that accumulation of AGEs accelerate the multisystem functional decline that occurs with aging, and therefore contribute to the aging phenotype. Exposure to AGEs can be reduced by restriction of dietary intake of AGEs and drug treatment with AGE inhibitors and AGE breakers. Modification of intake and circulating levels of AGEs may be a possible strategy to promote health in old age, especially because most Western foods are processed at high temperature and are rich in AGEs.
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AGEs have been linked to ageing, chronic illness and death, and they may contribute importantly to frailty.
“They have been associated with ageing, chronic disease and mortality and may have an important role in frailty (60).”
From Frailty in elderly people (2013) · cites this paper as [60]
Advanced glycation end products form when proteins, lipids and nucleic acids are glycated; they can damage cells widely by increasing inflammation.
“Advanced glycation end products (AGEs) are a group of molecules produced by the glycation of proteins, lipids and nucleic acid that have potential to cause widespread cellular damage by upregulation of inflammation (60).”
From Frailty in elderly people (2013) · cites this paper as [60]
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Advanced glycation end products in senile diabetic and nondiabetic patients with cataract
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Semba, R. D., Fink, J. C., Sun, K., Bandinelli, S., Guralnik, J. M., & Ferrucci, L. (2008) · European Journal of Nutrition · doi:10.1007/s00394-008-0757-0 · Cited by 47 · see citing works
Self-citationSouthern, L., Williams, J. H., & Esiri, M. M. (2007) · BMC Neurology · doi:10.1186/1471-2377-7-35 · Cited by 47 · see citing works
Cross-link breakers as a new therapeutic approach to cardiovascular disease
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Are dietary AGEs/ALEs a risk to human health and, if so, what is the mechanism of action?
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Self-citationMitochondrial hyperpolarization and ATP depletion in patients with systemic lupus erythematosus
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Flagged first, then by citations
Research works printed but not linked: 3
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Proteomics in aging research: A roadmap to clinical, translational research
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Self-citationYacoub, R., Nugent, M., Cai, W., Nadkarni, G. N., Chaves, L. D., Abyad, S., Honan, A. M., Thomas, S. A., Zheng, W., Valiyaparambil, S. A., et al. (2017) · PLOS ONE · doi:10.1371/journal.pone.0184789 · Cited by 139 · see citing works
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- Authors
- Semba, R. D., Nicklett, E. J., & Ferrucci, L.
- Affiliations
- Johns Hopkins University (US)
- University of Michigan (US)
- National Institute on Aging (US)
- Venue
- The Journals of Gerontology Series A: Biological Sciences and Medical Sciences
- Publisher
- Oxford University Press (OUP)
- Published
- 2010-05-17
- Volume
- 65A
- Issue
- 9
- Pages
- 963-975
- ISSN
- 1079-5006 (ISSN-L)
- 1758-535X
- PMC
- PMC2920582
- OpenAlex
- W2100383922
- Cited by
- 490
- References
- 111
- Citations by year
- 2026: 23 · 2025: 31 · 2024: 31 · 2023: 36 · 2022: 37 · 2021: 32 · 2020: 29 · 2019: 40 · 2018: 35 · 2017: 44 · 2016: 31 · 2015: 31 · 2014: 27 · 2013: 20 · 2012: 23
- FWCI
- 2.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journals of Gerontology Series A (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r37ag019905-10, NIH-R01, AG027012)
- National Institute on Aging (R37-AG019905, R01AG027012, R01AG029148)
- National Heart, Lung, and Blood Institute (R01HL094507)
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- advanced glycation end products, aging, glycation, inflammation, collagen cross-linking, chronic disease risk, dietary AGEs, AGE inhibitors, glucose metabolism, functional decline in older adults
- MeSH terms
- Receptor for Advanced Glycation End Products, Aging, Bone and Bones, Brain, Diet, Enzyme Inhibitors, Erythrocytes, Eye, Food Analysis, Guanidines, Humans, Inflammation, Kidney, Liver, Longevity, Myocardium, Receptors, Immunologic, Tendons, Thiazoles, Glycation End Products, Advanced, Oxidative Stress, Muscle, Skeletal
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