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.

Original languageEnglish
Pages (from-to)170-171
Number of pages2
JournalMolecular cell
Issue number2
StatePublished - Oct 21 2011


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