Mitochondrial SIRT3: a new potential therapeutic target for metabolic syndrome

Jun Yoshino; Shin-ichiro Imai

doi:10.1016/j.molcel.2011.10.005

Mitochondrial SIRT3: a new potential therapeutic target for metabolic syndrome

Mol Cell. 2011 Oct 21;44(2):170-1. doi: 10.1016/j.molcel.2011.10.005.

Authors

Jun Yoshino¹, Shin-ichiro Imai

Affiliation

¹ Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 63110, USA.

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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