Autophagy and Aging

被引：1748

作者：

Rubinsztein, David C. ^{[1
]}

Marino, Guillermo ^{[2
,3
,4
]}

Kroemer, Guido ^{[2
,3
,5
,6
,7
]}

机构：

[1] Univ Cambridge, Addenbrookes Hosp, Dept Med Genet, Cambridge Inst Med Res, Cambridge CB2 0XY, England

[2] INSERM, U848, F-94805 Villejuif, France

[3] Inst Gustave Roussy, F-94805 Villejuif, France

[4] Univ Paris Sud, F-94805 Villejuif, France

[5] Ctr Rech Cordeliers, F-75006 Paris, France

[6] Hop Europeen Georges Pompidou, AP HP, F-75015 Paris, France

[7] Univ Paris 05, Fac Med, F-75006 Paris, France

来源：

CELL | 2011年 / 146卷 / 05期

基金：

英国医学研究理事会; 英国惠康基金;

关键词：

LIFE-SPAN EXTENSION; BETA-CELL MASS; CALORIC RESTRICTION; MEDIATED AUTOPHAGY; MAMMALIAN AUTOPHAGY; DIETARY RESTRICTION; PROTEIN-SYNTHESIS; LONGEVITY; DISEASE; STRESS;

D O I：

10.1016/j.cell.2011.07.030

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Genetic inhibition of autophagy induces degenerative changes in mammalian tissues that resemble those associated with aging, and normal and pathological aging are often associated with a reduced autophagic potential. Pharmacological or genetic manipulations that increase life span in model organisms often stimulate autophagy, and its inhibition compromises the longevity-promoting effects of caloric restriction, Sirtuin 1 activation, inhibition of insulin/insulin growth factor signaling, or the administration of rapamycin, resveratrol, or spermidine. Here, we discuss the probable cause and effect relationship between perturbed autophagy and aging, as well as possible molecular mechanisms that may mediate the anti-aging effects of autophagy.

引用

收藏

页码：682 / 695

页数：14

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