MTOR and cardiac hypertrophy: The fact that only Akt-I was able to prevent the PE-induced increase in hypertrophic markers and protein synthesis, probably through direct links of Akt with HDAC5 [35] and mTOR, while both compounds were able to restore contractile function, indicates that the metabolic alterations upon development of cardiac hypertrophy are most likely of greater relevance in the development of cardiac dysfunction (Figure 7).