Cited by 142Genetics, Aging, and Longevity in Model OrganismsGenetic Associations and EpidemiologyGenetics and Physical Performance

Genetics of Longevity and Aging

Vijg, Jan, Suh, Yousin·2005·Annual Review of Medicine

Abstract

Longevity, i.e., the property of being long-lived, has its natural limitation in the aging process. Longevity has a strong genetic component, as has become apparent from studies with a variety of organisms, from yeast to humans. Genetic screening efforts with invertebrates have unraveled multiple genetic pathways that suggest longevity is promoted through the manipulation of metabolism and the resistance to oxidative stress. To some extent, these same mechanisms appear to act in mammals also, despite considerable divergence during evolution. Thus far, evidence from population-based studies with humans suggests the importance of genes involved in cardiovascular disease as important determinants of longevity. The challenge is to test if the candidate longevity genes that have emerged from studies with model organisms exhibit genetic variation for life span in human populations. Future investigations are likely to involve large-scale case-control studies, in which large numbers of genes, corresponding to entire gene functional modules, will be assessed for all possible sequence variation and associated with detailed phenotypic information on each individual over extended periods of time. This should eventually unravel the genetic factors that contribute to each particular aging phenotype.

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Crossref · 10.1146/annurev.med.56.082103.104617

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  • Genes that regulate lifespan in animal models and human studies, and multiple experimental paradigms, have demonstrated that it is possible to manipulate ageing biology to rejuvenate physiological functioning in complex model organisms.

    “Genes that regulate lifespan in animal models6–9 and human studies10–14 as well as multiple experimental paradigms, such as caloric restriction, heterochronic parabiosis and partial epigenetic reprogramming, have demonstrated that it is possible to manipulate ageing biology to ‘rejuvenate’ physiological functioning in complex model organisms15–28.”

    From Measuring biological age using omics data (2022) · cites this paper as [6]

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Authors
Vijg, J., & Suh, Y.
Affiliations
The University of Texas at San Antonio Health Science Center (US)
Venue
Annual Review of Medicine
Published
2005-02-01
Volume
56
Issue
1
Pages
193-212
ISSN
  • 0066-4219 (ISSN-L)
  • 1545-326X
OpenAlex
W2148208805
Cited by
142
References
94
Citations by year
2026: 1 · 2025: 1 · 2024: 2 · 2023: 3 · 2022: 1 · 2021: 7 · 2020: 3 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 14 · 2015: 6 · 2014: 4 · 2013: 13 · 2012: 10
FWCI
0.92
Type
journal article
Language
en
Open access
closed
Locations
  • Annual Review of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health
  • National Institute on Aging (AG 17242, AG23292, R01AG020438, R01AG024391, R03AG023292, AG 20438, P01AG017242)
  • National Institute of Environmental Health Sciences (ES 11044, U01ES011044)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetics and Physical Performance
Keywords
longevity, aging, longevity genes, oxidative stress resistance, metabolism, cardiovascular disease genes, model organisms, case-control study, aging phenotypes
MeSH terms
Aging, Animals, Cardiovascular Diseases, Biological Evolution, Humans, Insulin, Longevity, Phenotype, Genetic Variation, Signal Transduction, Case-Control Studies, Oxidative Stress

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