The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Delayed ageing through damage protection by the Arf/p53 pathway
Abstract
The tumour-suppressor pathway formed by the alternative reading frame protein of the Cdkn2a locus (Arf) and by p53 (also called Trp53) plays a central part in the detection and elimination of cellular damage, and this constitutes the basis of its potent cancer protection activity. Similar to cancer, ageing also results from the accumulation of damage and, therefore, we have reasoned that Arf/p53 could have anti-ageing activity by alleviating the load of age-associated damage. Here we show that genetically manipulated mice with increased, but otherwise normally regulated, levels of Arf and p53 present strong cancer resistance and have decreased levels of ageing-associated damage. These observations extend the protective role of Arf/p53 to ageing, revealing a previously unknown anti-ageing mechanism and providing a rationale for the co-evolution of cancer resistance and longevity.
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In the citing paper
“A moderate enhancement of the senescence-inducing tumor suppressor pathways may extend longevity”
From The Hallmarks of Aging (2013) · cites this paper as Matheu et al., 2007
In the citing paper
“mice with a mild and systemic increase in p16Ink4a, p19Arf or p53 tumor suppressors exhibit extended longevity, which cannot be accounted for by their lower cancer incidence”
From The Hallmarks of Aging (2013) · cites this paper as Matheu et al., 2007
In the citing paper
“mice in which both p53 and p19Arf are overexpressed show delayed ageing 32”
From The common biology of cancer and ageing (2007) · cites this paper as [32]
Citations
Cites
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Statistical analysis of real-time PCR data
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The p53 pathway: positive and negative feedback loops
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p53 mutant mice that display early ageing-associated phenotypes
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The antioxidant function of the p53 tumor suppressor
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Stem-cell ageing modified by the cyclin-dependent kinase inhibitor p16INK4a
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Cellular Senescence in Aging Primates
Herbig, U., Ferreira, M., Condel, L., Carey, D., & Sedivy, J. M. (2006) · Science · doi:10.1126/science.1122446 · Cited by 1,101
Cited by
Sorted by citations
López-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
Self-citationBlinded by the Light: The Growing Complexity of p53
Vousden, K. H., & Prives, C. (2009) · Cell · doi:10.1016/j.cell.2009.04.037 · Cited by 3,163
The role of senescent cells in ageing
van Deursen, J. M. (2014) · Nature · doi:10.1038/nature13193 · Cited by 2,623
Four faces of cellular senescence
Rodier, F., & Campisi, J. (2011) · Journal of Cell Biology · doi:10.1083/jcb.201009094 · Cited by 2,070
“Finally, mouse models without obvious activated DDR signaling also suggest that senescent cells can drive aging phenotypes.”
InfluentialAgeing as a Risk Factor for Disease
Niccoli, T., & Partridge, L. (2012) · Current Biology · doi:10.1016/j.cub.2012.07.024 · Cited by 1,831
Metadata
- Authors
- Matheu, A., Maraver, A., Klatt, P., Flores, I., Garcia-Cao, I., Borras, C., Flores, J. M., Viña, J., Blasco, M. A., & Serrano, M.
- Affiliations
- Spanish National Cancer Research Centre (ES)
- Universidad Complutense de Madrid (ES)
- Corresponding author
- Serrano, Manuel
- Venue
- Nature
- Published
- 2007-07
- Volume
- 448
- Issue
- 7151
- Pages
- 375-379
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1988008469
- Semantic Scholar
- 37a3bdfa93d3f09de784a1f376300624e93ff8d6
- Cited by
- 466
- References
- 38
- Citations by year
- 2026: 2 · 2025: 6 · 2024: 11 · 2023: 6 · 2022: 15 · 2021: 20 · 2020: 14 · 2019: 19 · 2018: 16 · 2017: 21 · 2016: 25 · 2015: 21 · 2014: 21 · 2013: 39 · 2012: 40
- FWCI
- 14.60
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Keywords
- ARF-p53 pathway, cellular aging, lifespan extension, tumor resistance, tumor suppression, CDKN2A, antioxidant activity, longevity
- MeSH terms
- Aging, Animals, Antioxidants, Cells, Cultured, Disease Susceptibility, Fibroblasts, Longevity, Neoplasms, Time Factors, Tumor Suppressor Protein p53, Oxidative Stress, Cyclin-Dependent Kinase Inhibitor p16, Mice
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