In addition, many preclinical studies have documented that the expression of miR-132 in the myocardium is up-regulated under various cardiac stresses and drives some basic pathological processes of heart failure, such as cardiac hypertrophy, fibrosis, and impaired calcium handling, through downregulation of FOXO3A, SERCA2a, PTEN, SIRT1 and other target gene expression, while targeted inhibition of miR-132 by antimiR-132 attenuates cardiac hypertrophy and improves cardiac function (Figure 1). This evidence concerns the gene FOXO3 and cardiac hypertrophy.