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Cell Metab. 2013 Dec 3;18(6):792-801. doi: 10.1016/j.cmet.2013.08.018. Epub 2013 Sep 19.

Sestrins orchestrate cellular metabolism to attenuate aging.

Author information

1
Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, MI 48109, USA.
2
Department of Human and Molecular Genetics, Virginia Commonwealth University, Richmond, VA 23298, USA.
3
Laboratory of Gene Regulation and Signal Transduction, Departments of Pharmacology and Pathology University of California, San Diego, San Diego, CA 92093, USA.
#
Contributed equally

Abstract

The Sestrins constitute a family of evolutionarily conserved stress-inducible proteins that suppress oxidative stress and regulate AMP-dependent protein kinase (AMPK)-mammalian target of rapamycin (mTOR) signaling. By virtue of these activities, the Sestrins serve as important regulators of metabolic homeostasis. Accordingly, inactivation of Sestrin genes in invertebrates resulted in diverse metabolic pathologies, including oxidative damage, fat accumulation, mitochondrial dysfunction, and muscle degeneration, that resemble accelerated tissue aging. Likewise, Sestrin deficiencies in mice led to accelerated diabetic progression upon obesity. Further investigation of Sestrin function and regulation should provide new insights into age-associated metabolic diseases, such as diabetes, myopathies, and cancer.

PMID:
24055102
PMCID:
PMC3858445
DOI:
10.1016/j.cmet.2013.08.018
[Indexed for MEDLINE]
Free PMC Article

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