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Reduced Expression of MYC Increases Longevity and Enhances Healthspan
Open accessAbstract
MYC is a highly pleiotropic transcription factor whose deregulation promotes cancer. In contrast, we find that Myc haploinsufficient (Myc(+/-)) mice exhibit increased lifespan. They show resistance to several age-associated pathologies, including osteoporosis, cardiac fibrosis, and immunosenescence. They also appear to be more active, with a higher metabolic rate and healthier lipid metabolism. Transcriptomic analysis reveals a gene expression signature enriched for metabolic and immune processes. The ancestral role of MYC as a regulator of ribosome biogenesis is reflected in reduced protein translation, which is inversely correlated with longevity. We also observe changes in nutrient and energy sensing pathways, including reduced serum IGF-1, increased AMPK activity, and decreased AKT, TOR, and S6K activities. In contrast to observations in other longevity models, Myc(+/-) mice do not show improvements in stress management pathways. Our findings indicate that MYC activity has a significant impact on longevity and multiple aspects of mammalian healthspan.
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“Among the Yamanaka factors, c-Myc is an oncogene that reduces mouse lifespan20 and is not required for the initiation of cellular reprogramming21.”
From Reprogramming to recover youthful epigenetic information and restore vision (2020) · cites this paper as [20]
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Metadata
- Authors
- Hofmann, J. W., Zhao, X., De Cecco, M., Peterson, A. L., Pagliaroli, L., Manivannan, J., Hubbard, G. B., Ikeno, Y., Zhang, Y., Feng, B., Li, X., Serre, T., Qi, W., Van Remmen, H., Miller, R. A., Bath, K. G., de Cabo, R., Xu, H., Neretti, N., & Sedivy, J. M.
- Affiliations
- Brown University (US)
- The University of Texas at San Antonio Health Science Center (US)
- National Institute on Aging (US)
- University of Michigan (US)
- Corresponding author
- Sedivy, John M.
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2015-01
- Volume
- 160
- Issue
- 3
- Pages
- 477-488
- ISSN
- 0092-8674 (ISSN-L)
- PMC
- PMC4624921
- OpenAlex
- W2019755675
- Cited by
- 293
- References
- 118
- Citations by year
- 2026: 12 · 2025: 21 · 2024: 23 · 2023: 35 · 2022: 30 · 2021: 34 · 2020: 38 · 2019: 24 · 2018: 17 · 2017: 24 · 2016: 21 · 2015: 14
- FWCI
- 10.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Cell (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- U.S. Department of Veterans Affairs (I01 BX002595)
- National Institutes of Health (1s10od016366-01, 5p42es013660-14)
- National Institute on Aging (R37AG016694, P01AG031736, F30AG035592, R01AG016694, P30AG024824, U01AG022303)
- National Institute of General Medical Sciences (P30GM103410)
- National Institute of Environmental Health Sciences (P42ES013660),)
- 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 › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- c-Myc, haploinsufficiency, longevity, healthspan, aging, ribosome biogenesis, mRNA translation, insulin-like growth factor I, AMPK, TOR signaling, S6K, immunosenescence, myocardial fibrosis, osteoporosis, lipid metabolism, metabolic rate, energy sensing
- MeSH terms
- Aging, Animals, Female, Longevity, Lymphoma, Male, Mice, Inbred C57BL, Proto-Oncogene Proteins c-myc, Body Size, Mice, Metabolic Networks and Pathways, Mice, 129 Strain, Transcriptome
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