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The genetics of ageing
Abstract
The nematode Caenorhabditis elegans ages and dies in a few weeks, but humans can live for 100 years or more. Assuming that the ancestor we share with nematodes aged rapidly, this means that over evolutionary time mutations have increased lifespan more than 2,000-fold. Which genes can extend lifespan? Can we augment their activities and live even longer? After centuries of wistful poetry and wild imagination, we are now getting answers, often unexpected ones, to these fundamental questions.
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“Genome wide expression profiling studies have identified several genes and biological pathways affected by aging (Bishop et al. 2010, Lopez-Otin et al. 2013, Kenyon 2010, Yankner et al. 2008).”
From miR‐186 is decreased in aged brain and suppresses BACE 1 expression (2016) · cites this paper as Kenyon 2010
In the citing paper
“Genetic polymorphisms or mutations that reduce the functions of GH, IGF-1 receptor, insulin receptor or downstream intracellular effectors such as AKT, mTOR and FOXO, have been linked to longevity, both in humans and in model organisms”
From The Hallmarks of Aging (2013) · cites this paper as Kenyon, 2010
In the citing paper
“autophagy induction is probably not the sole mechanism through which a healthy lifestyle can retard aging”
From The Hallmarks of Aging (2013) · cites this paper as Kenyon, 2010
In the citing paper
“Remarkably, the IIS pathway is the most conserved aging-controlling pathway in evolution”
From The Hallmarks of Aging (2013) · cites this paper as Kenyon, 2010
In the citing paper
“In vitro experiments show that mutations that reduce insulin/IGF-1 signaling have been shown to decelerate the degenerative aging process and extend lifespan in many organisms, including mice and possibly humans.”
From GHK and DNA: Resetting the human genome to health (2014) · cites this paper as [63]
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“Amino acid and energy metabolism in longevity There is evidence that the pathways mediating longevity in dietary restriction are engaged differently by different dietary restriction regimens (Greer et al., 2007a; Panowski et al., 2007; Greer & Brunet, 2009; Kenyon, 2010).”
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Metadata
- Authors
- Kenyon, C. J.
- Affiliations
- University of California, San Francisco (US)
- Corresponding author
- Kenyon, Cynthia J.
- ORCID
- Kenyon, Cynthia J.
- Venue
- Nature
- Published
- 2010-03-24
- Volume
- 464
- Issue
- 7288
- Pages
- 504-512
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W2058484936
- Cited by
- 2,739
- References
- 104
- Citations by year
- 2026: 106 · 2025: 115 · 2024: 130 · 2023: 128 · 2022: 149 · 2021: 182 · 2020: 198 · 2019: 189 · 2018: 173 · 2017: 185 · 2016: 190 · 2015: 194 · 2014: 202 · 2013: 197 · 2012: 181
- FWCI
- 15.05
- Type
- journal article
- Language
- en
- Update notices
- erratum (2010-09-29)
- Open access
- closed
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Funders
- Tokyo Center for Economic Research
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Keywords
- aging, lifespan extension, Caenorhabditis elegans, longevity genes, human lifespan
- MeSH terms
- Aging, Animals, Humans, Insulin, Insulin-Like Growth Factor I, Longevity, Transferases, Signal Transduction, Cell Respiration
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