Extending healthy life span--from yeast to humans.

Extending healthy life span--from yeast to humans.
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DOI:
10.1126/science.1172539
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发表时间:
2010-04-16
期刊:
Science (New York, N.Y.)
影响因子:
--
通讯作者:
Longo VD
Longo VD
中科院分区:
其他
文献类型:
--
作者:
Fontana L;Partridge L;Longo VD

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饮食限制(DR)和减少生长因子信号都能提高模式生物对氧化应激的抵抗力,减少大分子损伤,延长寿命。在啮齿类动物中,DR和减少的生长因子信号都能降低肿瘤的发生率,减缓认知能力下降和衰老。DR减少了猴子的癌症和心血管疾病以及死亡率,并减少了人类与糖尿病、心血管疾病和癌症相关的代谢特征。肿瘤和糖尿病在生长激素受体功能突变丧失的人类中也很少见。因此,DR和减少的生长因子信号可能通过类似的、进化保守的机制来延缓衰老。我们回顾了模式生物中这些保守的抗衰老途径,讨论了它们与哺乳动物疾病预防的联系,并考虑了可能阻碍旨在延长人类健康寿命的干预措施的负面副作用。
Dietary restriction (DR) and reduced growth factor signaling both elevate resistance to oxidative stress, reduce macromolecular damage, and increase lifespan in model organisms. In rodents, both DR and decreased growth factor signaling reduce the incidence of tumors and slow down cognitive decline and aging. DR reduces cancer and cardiovascular disease and mortality in monkeys, and reduces metabolic traits associated with diabetes, cardiovascular disease and cancer in humans. Neoplasias and diabetes are also rare in humans with loss of function mutations in the growth hormone receptor. DR and reduced growth factor signaling may thus slow aging by similar, evolutionarily conserved, mechanisms. We review these conserved anti-aging pathways in model organisms, discuss their link to disease prevention in mammals, and consider the negative side effects that might hinder interventions intended to extend healthy lifespan in humans.
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