Mitochondrial sirtuins in the heart
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Updated: Mar 19, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins SIRT2 and Specific Protein-substrates
Published on: February 27, 2016
Heiko Bugger1, Constantin N Witt2, Christoph Bode2
1Department of Cardiology and Angiology I, Heart Center Freiburg University, Hugstetter Str. 55, 79106, Freiburg, Germany. heiko.bugger@universitaets-herzzentrum.de.
Abstract:
Sirtuins (SIRTs) are NAD(+)-dependent enzymes that catalyze deacylation of protein lysine residues. In mammals, seven sirtuins have been identified, SIRT1-7. SIRT3-5 are mainly or exclusively localized within mitochondria and mainly participate in the regulation of energy metabolic pathways. Since mitochondrial ATP regeneration is inevitably linked to the maintenance of cardiac pump function, it is not surprising that recent studies revealed a role for mitochondrial sirtuins in the regulation of myocardial energetics and function. In addition, mitochondrial sirtuins modulate the extent of myocardial ischemia reperfusion injury and the development of cardiac hypertrophy and failure. Thus, targeting mitochondrial sirtuins has been proposed as a novel approach to improve myocardial mitochondrial energetics, which is frequently impaired in cardiac disease and considered an important underlying cause contributing to several cardiac pathologies, including myocardial ischemia reperfusion injury and heart failure. In the current review, we present and discuss the available literature on mitochondrial sirtuins and their potential roles in cardiac physiology and disease.
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