Dissemin is shutting down on January 1st, 2025

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Taylor and Francis Group, Cell Cycle, 22(11), p. 4135-4146, 2012

DOI: 10.4161/cc.22074

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Sirt1: Def-eating senescence?

Journal article published in 2012 by Salvatore Fusco ORCID, Giuseppe Maulucci ORCID, Giovambattista Pani
This paper is available in a repository.
This paper is available in a repository.

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Data provided by SHERPA/RoMEO

Abstract

Sirt1, the closest mammalian homolog of the Sir2 yeast longevity protein, has been extensively investigated in the last few years as an avenue to understand the connection linking nutrients and energy metabolism with aging and related diseases. From this research effort the picture has emerged of an enzyme at the hub of a complex array of molecular interactions whereby nutrient-triggered signals are translated into several levels of adaptive cell responses, the failure of which underlies diseases as diverse as diabetes, neurodegeneration and cancer. Sirt1 thus connects moderate calorie intake to “healthspan,” and a decline of Sirt-centered protective circuits over time may explain the “catastrophic” nature of aging.