Evidence map›Paper›PMID 8340104›Full record

ReviewHuman genetics1993

Prospects for the genetics of human longevity.

F Schächter, D Cohen, T Kirkwood

Abstract readReview
PubMed Publisher
In one paragraph

Review in Human genetics, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
1.2field-weighted citation impact, top 21% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Genetic cartography of longevity in humans and mice: Current landscape and horizons.Biochimica et biophysica acta. Molecular basis of disease · 2018
    Review
  4. A Genetic Network Associated With Stress Resistance, Longevity, and Cancer in Humans.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016
    Article
  5. Article
  6. Article
  7. Growing up in ageing.Clinical medicine (London, England) · 2011
    Article
  8. Article
  9. Article
  10. Article
  11. Zinc, infections and immunosenescence.Mechanisms of ageing and development · 2000
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. The origins of human ageing.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1997
    Review
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

F SchächterCentre d'Etude du Polymorphisme Humain, Paris, France.
D Cohen
T Kirkwood
Fondation Jean Dausset-CEPH · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Longevity varies between and within species. The existence of species-specific limit to human life-span and its partial heritability indicate the existence of genetic factors that influence the ageing process. Insight into the nature of these genetic factors is provided by evolutionary studies, notably the disposable soma theory, which suggests a central role of energy metabolism in determining life-span. Energy is important in two ways. First, the disposable soma theory indicates that the optimum energy investment in cell maintenance and repair processes will be tuned through natural selection to provide adequate, but not excessive, protection against random molecular damages (e.g. to DNA, proteins). All that is required is that the organism remains in a sound condition through its natural expectation of life in the wild environment, where accidents are the predominant cause of mortality. Secondly, energy is implicated because of the intrinsic vulnerability of mitochondria to damage that may interfere with the normal supply of energy to the cell via the oxidative phosphorylation pathways. Oxidative phosphorylation produces ATP, and as a by-product also produces highly reactive oxygen radicals that can damage many cell structures, including the mitochondria themselves. Several lines of evidence link, on the one hand, oxidative damage to cell ageing, and on the other hand, energy-dependent antioxidant defences to the preservation of cellular homeostasis, and hence, longevity. Models of cellular ageing in vitro allow direct investigation of mechanisms, such as oxidative damage, that contribute to limiting human life-span. The genetic substratum of inter-individual differences in longevity may be unraveled by a two-pronged reverse genetics approach: sibling pair analysis applied to nonagenarian and centenarian siblings, combined with association studies of centenarians, may lead to the identification of genetic influences upon human longevity. These studies have become practicable thanks to recent progress in human genome mapping, especially to the development of microsatellite markers and the integration of genetic and physical maps.

Indexed as

AgingCellular SenescenceEnergy MetabolismGenetic TechniquesHumansLongevityMitochondriaModels, BiologicalOxidative PhosphorylationPolymorphism, GeneticSpecies Specificity

Identifiers

PMID8340104
OpenAlexW2042185915

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.