Post-translational modification through acetylation by the NAD+-dependent deacetylase sirtuin-3, or SIRT3, has recently emerged as a key player in regulating mitochondrial function. What is SIRT3 doing in cardiac mitochondria? How does it impact cardiac physiology and pathophysiology? Listen as Editor in Chief William Stanley and Associate Editor Junichi Sadoshima talk with the author Michael Sack (National Heart, Lung and Blood Institute, NIH) about his just-published Review article which tackles these very questions.
Michael N. Sack. Emerging characterization of the role of SIRT3 mediated mitochondrial protein deacetylation in the heart. Am J Physiol Heart Circ Physiol, published ahead of print October 7, 2011, doi:10.1152/ajpheart.00199.2011.
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