Figure 3.

Cardiovascular effects of Sirt3. Mitochondrial Sirt3 drives the tricarboxylic acid cycle, β-oxidation, and oxidative phosphorylation, thus maintaining metabolic homeostasis and preventing the development of risk factors associated with the metabolic syndrome. Deacetylation and consecutive activation of superoxide dismutase 2 mediates antioxidative protection, diminishes cardiac hypertrophy, and may improve endothelial dysfunction. Activation of the transcription factors NFATc2, STAT3, and HIF1α prevent the development of pulmonary hypertension.