IGF1 and cardiac hypertrophy: Under stimulations, the myocardium shifts for higher energy demand, which occurs with the upregulation of IGF-1 and the decline of miR-1; (1) exposure to IGF-1 results in increased FABP3 expression, and (2) on the other hand, miR-1 downregulation is able to release its inhibitory role on FABP3 and eventually elicit the increase in FABP3 under cardiac hypertrophy (14).