Journal
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS
Volume 1790, Issue 10, Pages 1067-1074Publisher
ELSEVIER
DOI: 10.1016/j.bbagen.2009.06.007
Keywords
Aging; TOR; S6 kinase; Neurodegeneration; Metabolic syndrome; Cardiovascular disease; Dietary restriction
Categories
Funding
- NIA [R01AG033373-01A1, R01AG025549-04, R01AG031108]
- NIH [T32AG000057]
- NATIONAL INSTITUTE ON AGING [R01AG033373, T32AG000057, R01AG025549, R01AG031108] Funding Source: NIH RePORTER
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Studies in a variety of model organisms indicate that nutrient signaling is tightly coupled to longevity. In nutrient replete conditions, organisms develop, grow, and age quickly. When nutrients become sparse as with dietary restriction, growth and development decline, stress response pathways become induced and organisms live longer. Considerable effort has been devoted to understanding the molecular events mediating lifespan extension by dietary restriction. One central focus has been on nutrient-responsive signal transduction pathways including insulin/IGF-1, AMP kinase, protein kinase A and the TOR pathway. Here we describe the increasingly prominent links between TOR signaling and aging in invertebrates. Longevity studies in mammals are not published to date. Instead, we highlight studies in mouse models, which indicate that dampening the TOR pathway leads to widespread protection from an array of age-related diseases. (C) 2009 Elsevier B.V. All rights reserved.
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