Evidence for only two independent pathways for decreasing senescence in Caenorhabditis elegans

被引:21
作者
Yen, Kelvin [1 ]
Mobbs, Charles V. [2 ]
机构
[1] Univ Massachusetts, Sch Med, Worcester, MA 01606 USA
[2] Mt Sinai Sch Med, New York, NY 10029 USA
关键词
Caenorhabditis elegans; Aging; Lifespan; Gompertz analysis; GENE-EXPRESSION PROFILE; INCREASED LIFE-SPAN; DIETARY-RESTRICTION; OXIDATIVE STRESS; C-ELEGANS; METABOLIC-RATE; CALORIC RESTRICTION; SIGNALING PATHWAY; INSULIN-RECEPTOR; WILD-TYPE;
D O I
10.1007/s11357-009-9110-7
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
Cold temperature, dietary restriction, reduced insulin/insulin-like growth factor signaling, and mutations in mitochondrial genes have all been shown to extend the lifespan of Caenorhabditis elegans (Kenyon et al., Nature 366:461-464, 1993; Klass, Mech Ageing Dev 6:413-429, 1977; Lakowski and Hekimi, Science 272:1010-1013, 1996). Additionally, all of them extend the lifespan of mice (Bluher et al., Science 299:572-574, 2003; Conti et al., Science 314:825-828, 2006; Holzenberger et al., Nature 421:182-187, 2003; Liu et al., Genes Dev 19:2424-2434, 2005; Weindruch and Walford, Science 215:1415-1418, 1982). The mechanism by which these treatments extend lifespan is currently unknown, but our study uses an epistatic approach to show that these four manipulations are mainly additive in terms of lifespan. Classical interpretation of this data suggests that these manipulations are independent of each other. However, using a Gompertz mortality rate analysis, the maximum mortality rate doubling time can be achieved through the use of only dietary restriction and cold temperature, suggesting that the mechanisms by which cold temperature and caloric restriction extend lifespan are the only independent mechanisms.
引用
收藏
页码:39 / 49
页数:11
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