Taken together, as for the prevention or treatment of human HF, VNS provides a novel and promising clinical strategy through optimized energy metabolism and sarcomere organization of myocardium during the process of delaying and/or blocking the transition from compensated hypertrophy to decompensated HF, which were associated with activation of both P13K/AKT–FoxO3A–VEGF-A/B signaling cascade. Here, FOXO3 is linked to hydrops fetalis.