Linking sirtuins, IGF-I signaling, and starvation.

摘要: Our studies in yeast have shown that the down-regulation of major signal transduction mediators increases stress resistance and causes an up to 10 fold chronological life span extension. Whereas other laboratories proposed sirtuins (Sir2 its homologs), a family conserved proteins which are NAD(+)-dependent histone deacetylases, can extend longevity various model organisms, we propose one sirtuin, i.e., Sir2, also accelerate cellular aging death. In Saccharomyces cerevisiae (yeast), deletion Sir2 DNA damage but combination with mutations principal intracellular mediators, or calorie restriction it further increase lifespan as well reduction age-dependent genomic instability. recent results provide evidence for role mammalian ortholog SirT1 activation highly neuronal pathway sensitization neurons oxidative damage. However, mean SirT1(+/-) mice is not different from wild type animals, survival SirT1(-/-) was reduced under both normal restricted conditions. Here, I review linking SirT1, IGF-I signaling starvation organisms focus on post-mitotic cells, indicate play protective pro-aging roles.