Cited by 133Genetics, Aging, and Longevity in Model OrganismsTelomeres, Telomerase, and SenescenceEvolution and Genetic Dynamics

The evolutionary theories of aging revisited - a mini-review

Ljubuncic, Predrag, Reznick, Abraham Z.·2009·Gerontology

Abstract

This short review portrays the evolutionary theories of aging in the light of the existing discoveries from genomic and molecular genetic studies on aging and longevity. At the outset, an historical background for the development of the evolutionary theories of aging is presented through the works of August Weismann (programmed death and the germ plasm theories) including his exceptional theoretical postulation, later experimentally validated by the existence of cell division limits. Afterwards, the theory of mutation accumulation of Peter Medawar and the theory modification by Charlesworth (late-life mortality plateau) are presented as well as the antagonistic pleiotropy hypothesis of George Williams, and the disposable soma theory of Kirkwood and Holliday. These theories are discussed in the light of the different research studies, which include studies on insulin signaling and longevity, the possibility that nuclear factor kappa B may be a major mediator of aging, studies of anti-aging Sirtuins and studies on heat shock proteins and longevity and on gene sets as biomarkers of aging. Finally, the proposals for future research in biogerontology, such as studies on the control of protein synthesis, validation of biomarkers of aging, understanding the biochemistry of longevity and research in the field of gerontologic pathology are presented. Likewise, further attention is suggested regarding the work on telomere shortening, stem cells and studies on understanding the biochemical and molecular basis for longevity in centenarians.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1159/000200772

Cites

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Biological aging is the progressive manifestation of accumulated cellular damage with age, determined by environmental or genetic factors.

    “Biological aging is the progressive manifestation of accumulated cellular damage with age, and is determined by environmental or genetic factors”

    From Redox control of senescence and age-related disease. (2017) · cites this paper as [2]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

The citation lists haven’t been fetched yet

References 80 · Cited by 133

Research works printed but not linked: 1

  1. 1 Weismann A: Essays Upon Heredity. Oxford, Clarendon Press, 1891.

Authors
Ljubuncic, P., & Reznick, A. Z.
Affiliations
Technion – Israel Institute of Technology (IL)
Venue
Gerontology
Publisher
S. Karger AG
Published
2009
Volume
55
Issue
2
Pages
205-216
ISSN
  • 0304-324X (ISSN-L)
  • 1423-0003
OpenAlex
W2061442557
Cited by
133
References
80
Citations by year
2026: 3 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 4 · 2021: 25 · 2020: 4 · 2019: 6 · 2018: 6 · 2017: 8 · 2016: 9 · 2015: 4 · 2014: 11 · 2013: 18 · 2012: 7
FWCI
0.96
Type
journal article
Language
en
Open access
closed
Locations
  • Gerontology (publishedVersion)
  • PubMed (publishedVersion)
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
programmed death, mutation accumulation theory, antagonistic pleiotropy, disposable soma theory, insulin signaling, NF-κB, sirtuins, heat shock proteins, aging biomarkers, gene sets, telomere shortening, stem cells, centenarians, longevity
MeSH terms
Aged, Aged, 80 and over, Aging, Animals, Biological Evolution, Heat-Shock Proteins, Humans, Insulin, Longevity, Models, Biological, Models, Genetic, Molecular Biology, Mutation, Selection, Genetic, Signal Transduction, NF-kappa B, Sirtuins, Electron Transport Chain Complex Proteins

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review