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Bugger, H; Witt, CN; Bode, C.
Mitochondrial sirtuins in the heart.
Heart Fail Rev. 2016; 21(5): 519-528. Doi: 10.1007/s10741-016-9570-7
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Führende Autor*innen der Med Uni Graz
Bugger Heiko Matthias
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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.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Energy Metabolism -
Heart Failure - etiology
Humans -
Mice -
Mitochondria, Heart - metabolism
Myocardial Reperfusion Injury - etiology
Sirtuin 3 - genetics
Sirtuin 3 - physiology

Find related publications in this database (Keywords)
Sirtuin
Mitochondria
Ischemia reperfusion
Heart failure
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