Calorie restriction Decelerating mTOR-driven aging from cells to organisms (including humans)

被引:178
作者
Blagosklonny, Mikhail V. [1 ]
机构
[1] Roswell Pk Canc Inst, Dept Cell Stress Biol, Buffalo, NY 14263 USA
关键词
aging; rapamycin; senescence; mTOR; calorie restriction; diseases; obesity; ACTIVATED PROTEIN-KINASE; CHRONOLOGICAL LIFE-SPAN; OXIDATIVE DAMAGE THEORY; DIET-INDUCED OBESITY; INSULIN-RESISTANCE; MAMMALIAN TARGET; DOWN-REGULATION; C; ELEGANS; AMINO-ACID; S6; KINASE;
D O I
10.4161/cc.9.4.10766
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Although it has been known since 1917 that calorie restriction (CR) decelerates aging, the topic remains highly controversial. What might be the reason? Here I discuss that the anti-aging effect of CR rules out accumulation of DNA damage and failure of maintenance as a cause of aging. Instead, it suggests that aging is driven in part by the nutrient-sensing TOR (target of rapamycin) network. CR deactivates the TOR pathway, thus slowing aging and delaying diseases of aging. Humans are not an exception and CR must increase both maximal and healthy lifespan in humans to the same degree as it does in other mammals. Unlike mice, however, humans benefit from medical care, which prolongs lifespan despite accelerated aging in non-restricted individuals. Therefore in humans the effect of CR may be somewhat blunted. Still how much does CR extend human lifespan? And could this extension be surpassed by gerosuppressants such as rapamycin?
引用
收藏
页码:683 / 688
页数:6
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