Signaling Networks Determining Life Span.
The health of an organism is orchestrated by a multitude of molecular and biochemical networks responsible for ensuring homeostasis within cells and tissues. However, upon aging, a progressive failure in the maintenance of this homeostatic balance occurs in response to a variety of endogenous and environmental stresses, allowing the accumulation of damage, the physiological decline of individual tissues, and susceptibility to diseases. What are the molecular and cellular signaling events that control the aging process and how can this knowledge help design therapeutic strategies to combat age-associated diseases? Here we provide a comprehensive overview of the evolutionarily conserved biological processes that alter the rate of aging and discuss their link to disease prevention and the extension of healthy life span.
Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; email: dillin@berkeley.edu.|Howard Hughes Medical Institute, Chevy Chase, Maryland 20815.|Glenn Center for Research on Aging, University of California, Berkeley, California 94720.
Celine E
CE
Riera
Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; email: dillin@berkeley.edu.|Howard Hughes Medical Institute, Chevy Chase, Maryland 20815.|Glenn Center for Research on Aging, University of California, Berkeley, California 94720.
Carsten
C
Merkwirth
Howard Hughes Medical Institute, Chevy Chase, Maryland 20815.|The Salk Institute for Biological Studies, La Jolla, California 92037.
C Daniel
CD
De Magalhaes Filho
Department of Molecular and Cell Biology, University of California, Berkeley, California 94720; email: dillin@berkeley.edu.|Howard Hughes Medical Institute, Chevy Chase, Maryland 20815.|Glenn Center for Research on Aging, University of California, Berkeley, California 94720.
Andrew
A
Dillin
D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism; D000818:Animals; D031204:Caloric Restriction; D004249:DNA Damage; D044127:Epigenesis, Genetic; D006706:Homeostasis / Q000235:genetics; D006801:Humans; D007249:Inflammation; D007334:Insulin-Like Growth Factor I / Q000235:genetics / Q000378:metabolism; D008136:Longevity / Q000235:genetics*; D008928:Mitochondria / Q000378:metabolism; D018384:Oxidative Stress; D057165:Proteostasis Deficiencies / Q000235:genetics* / Q000378:metabolism / Q000473:pathology; D015398:Signal Transduction; D058570:TOR Serine-Threonine Kinases / Q000235:genetics / Q000378:metabolism; D059506:Telomere Shortening
D007334:Insulin-Like Growth Factor I; C546842:MTOR protein, human; D058570:TOR Serine-Threonine Kinases; D055372:AMP-Activated Protein Kinases
DNA damage; epigenetic regulation; inflammation; insulin-like signaling; mammalian aging; mitochondrial health; nutrient sensing; oxidative stress; proteostasis; telomere shortening