SIRT3 and heart failure: The shift towards a more oxidised mitochondrial NADH/NAD+-balance in tachycardiomyopathy corresponds to a favourable effect on mitochondrial protein acetylation: in other heart failure aetiologies, the pro-reductive mitochondrial redox-balance, characterised by increased NADH and diminished NAD+-levels, inhibits mitochondrial NAD+-dependent deacetylases, e.g., sirtuin 3 [45].