Mitochondrial SIRT3: a new potential therapeutic target for metabolic syndrome.
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.
Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
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