Mitochondrial SIRT3: a new potential therapeutic target for metabolic syndrome
Jun Yoshino1, Shin-ichiro Imai
1Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
Molecular Cell
|October 25, 2011
Abstract:
In this issue of Molecular Cell, Hirschey et al. demonstrate that loss of the NAD(+)-dependent deacetylase SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesis of metabolic syndrome, providing new insights into the therapeutic potential of SIRT3.
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