The TOR pathway comes of age

被引:264
作者
Stanfel, Monique N. [2 ]
Shamieh, Lara S. [1 ]
Kaeberlein, Matt [1 ]
Kennedy, Brian K. [2 ]
机构
[1] Univ Washington, Dept Pathol, Seattle, WA 98195 USA
[2] Univ Washington, Dept Biochem, Seattle, WA 98195 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-GENERAL SUBJECTS | 2009年 / 1790卷 / 10期
关键词
Aging; TOR; S6; kinase; Neurodegeneration; Metabolic syndrome; Cardiovascular disease; Dietary restriction; LIFE-SPAN EXTENSION; ACTIVATED PROTEIN-KINASE; DIETARY RESTRICTION; CALORIC RESTRICTION; MAMMALIAN TARGET; S6; KINASE; SIGNALING PATHWAY; CARDIAC-HYPERTROPHY; UP-REGULATION; INCREASED RESPIRATION;
D O I
10.1016/j.bbagen.2009.06.007
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
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.
引用
收藏
页码:1067 / 1074
页数:8
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