Why do we age?
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The evolutionary theory of ageing explains why ageing occurs, giving valuable insight into the mechanisms underlying the complex cellular and molecular changes that contribute to senescence. Such understanding also helps to clarify how the genome shapes the ageing process, thereby aiding the study of the genetic factors that influence longevity and age-associated diseases.
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Gatekeeper tumor suppressor mechanisms may be an example of evolutionary antagonistic pleiotropy.
“Thus, gatekeeper tumor suppressor mechanisms may be an example of evolutionary antagonistic pleiotropy (reviewed in Kirkwood and Austad [2000]; Campisi, 2003b).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Kirkwood and Austad [2000]
Cellular senescence is a program with both beneficial and detrimental effects on organismal health, considered an example of evolutionary antagonistic pleiotropy.
“It is a cellular program which acts as a double-edged sword, with both beneficial and detrimental effects on the health of the organism, and considered to be an example of evolutionary antagonistic pleiotropy.”
From Mechanisms of Cellular Senescence: Cell Cycle Arrest and Senescence Associated Secretory Phenotype (2021) · cites this paper as Kirkwood and Austad, 2000
No positively selected programs exist for aging and chronic inflammatory diseases.
“Since no positively selected programs exist for aging [44] and chronic inflammatory diseases [8, 45]”
From Evolutionary medicine and chronic inflammatory state—known and new concepts in pathophysiology (2012) · cites this paper as [44]
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“]. The apparent paradox of contributing to both tumor suppression and aging is consistent with an evolutionary theory of aging, termed antagonistic pleiotropy [”
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- Authors
- Kirkwood, T. B. L., & Austad, S. N.
- Affiliations
- Newcastle University (GB)
- University of Idaho (US)
- Venue
- Nature
- Published
- 2000-11
- Volume
- 408
- Issue
- 6809
- Pages
- 233-238
- ISSN
- 0028-0836 (ISSN-L)
- 1476-4687
- OpenAlex
- W1658682427
- Cited by
- 1,774
- References
- 1
- Citations by year
- 2026: 48 · 2025: 62 · 2024: 42 · 2023: 55 · 2022: 54 · 2021: 81 · 2020: 52 · 2019: 70 · 2018: 77 · 2017: 77 · 2016: 77 · 2015: 80 · 2014: 81 · 2013: 84 · 2012: 51
- FWCI
- 4.06
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature (publishedVersion)
- PubMed (publishedVersion)
- RePEc: Research Papers in Economics (submittedVersion)
- Newcastle University ePrints (Newcastle Univesity)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Evolution and Genetic Dynamics
- Keywords
- senescence, aging mechanisms, longevity, age-related diseases
- MeSH terms
- Aging, Animals, Energy Intake, Biological Evolution, Humans, Models, Biological, Reproduction, Selection, Genetic
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