Literature DB >> 8914487

Hypothesis: interventions that increase the response to stress offer the potential for effective life prolongation and increased health.

T E Johnson1, G J Lithgow, S Murakami.   

Abstract

In the last decade it has become evident that many laboratory manipulations, both genetic and environmental, can lead to significant life extension. All or almost all of the observed life-extension phenotypes are associated with increased resistance and/or ability to respond to environmental stress. These observations show dramatically that life span is not maximized. We suggest that latent within many species-perhaps even humans-is the ability for large increases of life expectancy. The striking correlation between the increased stress resistance of all long-lived mutants in C. elegans and other species and the increased resistance of dietary restricted rodents to environmental toxins is consistent with an evolutionary conservation of a life-span maintenance/environmental stress resistance program. We suggest that it may be possible to develop methods for life extension in mammals, including humans, using relatively straightforward manipulations, such as drug treatments. It should be obvious that these findings have tremendous implications for human society at large, and we suggest that the implications of these findings should be explored.

Entities:  

Mesh:

Year:  1996        PMID: 8914487     DOI: 10.1093/gerona/51a.6.b392

Source DB:  PubMed          Journal:  J Gerontol A Biol Sci Med Sci        ISSN: 1079-5006            Impact factor:   6.053


  30 in total

Review 1.  Longevity genes in the nematode Caenorhabditis elegans also mediate increased resistance to stress and prevent disease.

Authors:  T E Johnson; S Henderson; S Murakami; E de Castro; S H de Castro; J Cypser; B Rikke; P Tedesco; C Link
Journal:  J Inherit Metab Dis       Date:  2002-05       Impact factor: 4.982

2.  Skin-derived fibroblasts from long-lived species are resistant to some, but not all, lethal stresses and to the mitochondrial inhibitor rotenone.

Authors:  James M Harper; Adam B Salmon; Scott F Leiser; Andrzej T Galecki; Richard A Miller
Journal:  Aging Cell       Date:  2006-12-05       Impact factor: 9.304

3.  Longevity determined by developmental arrest genes in Caenorhabditis elegans.

Authors:  Di Chen; Kally Z Pan; Julia E Palter; Pankaj Kapahi
Journal:  Aging Cell       Date:  2007-05-29       Impact factor: 9.304

Review 4.  Cell stress and aging: new emphasis on multiplex resistance mechanisms.

Authors:  Richard A Miller
Journal:  J Gerontol A Biol Sci Med Sci       Date:  2009-02-18       Impact factor: 6.053

5.  The Arabidopsis NAC transcription factor VNI2 integrates abscisic acid signals into leaf senescence via the COR/RD genes.

Authors:  So-Dam Yang; Pil Joon Seo; Hye-Kyung Yoon; Chung-Mo Park
Journal:  Plant Cell       Date:  2011-06-14       Impact factor: 11.277

Review 6.  Somatotropic signaling: trade-offs between growth, reproductive development, and longevity.

Authors:  Andrzej Bartke; Liou Y Sun; Valter Longo
Journal:  Physiol Rev       Date:  2013-04       Impact factor: 37.312

7.  SLR-2 and JMJC-1 regulate an evolutionarily conserved stress-response network.

Authors:  Natalia V Kirienko; David S Fay
Journal:  EMBO J       Date:  2010-01-07       Impact factor: 11.598

8.  Oxidative stress and longevity in Caenorhabditis elegans as mediated by SKN-1.

Authors:  Sang-Kyu Park; Patricia M Tedesco; Thomas E Johnson
Journal:  Aging Cell       Date:  2009-03-27       Impact factor: 9.304

9.  Oxidative damage, aging and anti-aging strategies.

Authors:  Ronny Haenold; D Mokhtar Wassef; Stefan H Heinemann; Toshinori Hoshi
Journal:  Age (Dordr)       Date:  2005-12-31

10.  Overexpression of the CBF2 transcriptional activator in Arabidopsis delays leaf senescence and extends plant longevity.

Authors:  Michal Sharabi-Schwager; Amnon Lers; Alon Samach; Charles L Guy; Ron Porat
Journal:  J Exp Bot       Date:  2010       Impact factor: 6.992

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