With TOR, Less Is More: A Key Role for the Conserved Nutrient-Sensing TOR Pathway in Aging

被引：510

作者：

Kapahi, Pankaj ^{[1
]}

Chen, Di ^{[1
]}

Rogers, Anc N. ^{[1
]}

Katewa, Subhash D. ^{[1
]}

Li, Patrick Wai-Lun ^{[1
]}

Thomas, Emma L. ^{[1
]}

Kockel, Lutz ^{[2
]}

机构：

[1] Buck Inst Age Res, Novato, CA 94945 USA

[2] Univ Calif San Francisco, Dept Med, Ctr Diabet, San Francisco, CA 94143 USA

来源：

CELL METABOLISM | 2010年 / 11卷 / 06期

基金：

美国国家卫生研究院;

关键词：

LIFE-SPAN EXTENSION; CELL-CYCLE ARREST; DIETARY RESTRICTION; AUTOPHAGY GENES; S6; KINASE; DEVELOPMENTAL ARREST; CALORIC RESTRICTION; STRESS RESISTANCE; HYPOXIC RESPONSE; RAG GTPASES;

D O I：

10.1016/j.cmet.2010.05.001

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Target of rapamycin (TOR) is an evolutionarily conserved nutrient-sensing protein kinase that regulates growth and metabolism in all eukaryotic cells. Studies in flies, worms, yeast, and mice support the notion that the TOR signaling network modulates aging. TOR is also emerging as a robust mediator of the protective effects of various forms of dietary restriction (DR), which can extend life span and slow the onset of certain age-related diseases across species. Here we discuss how modulating TOR signaling slows aging through downstream processes including mRNA translation, autophagy, endoplasmic reticulum (ER) stress signaling, stress responses, and metabolism. Identifying the mechanisms by which the TOR signaling network works as a pacemaker of aging is a major challenge and may help identify potential drug targets for age-related diseases, thereby facilitating healthful life span extension in humans.

引用

页码：453 / 465

页数：13

共 124 条

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