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

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...

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Bibliographic Details
Published in:Cell metabolism 2010-06, Vol.11 (6), p.453-465
Main Authors: Kapahi, Pankaj, Chen, Di, Rogers, Aric N., Katewa, Subhash D., Li, Patrick Wai-Lun, Thomas, Emma L., Kockel, Lutz
Format: Article
Language:English
Subjects:
Aging
Animals
Autophagy
Endoplasmic Reticulum - physiology
Humans
HUMDISEASE
Intracellular Signaling Peptides and Proteins - metabolism
Intracellular Signaling Peptides and Proteins - physiology
Longevity
Mice
Protein-Serine-Threonine Kinases - metabolism
Protein-Serine-Threonine Kinases - physiology
Ribosomal Protein S6 Kinases - metabolism
RNA, Messenger - metabolism
Signal Transduction
SIGNALING
TOR Serine-Threonine Kinases
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Summary: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.
ISSN:1550-4131
1932-7420
DOI:10.1016/j.cmet.2010.05.001