FOXO3 and systolic heart failure: BNIP3 monomer expression significantly increases in PE-stressed cardiomyocytes and in constitutively active FOXO3a expressing cardiomyocytes in vitro [17,26] and in animal models of myocardial remodeling and systolic dysfunction [13,14,17,26,27], in vivo, as well as in human systolic heart failure [15].