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Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.
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.
Copyright © 2011 Elsevier Inc. All rights reserved.
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