This study aimed to establish a model of pediatric heart failure (PHF) with concomitant left ventricle pressure overload by transverse aortic constriction (TAC) and study the PHF mechanism primarily at the gene transcription level.Twenty-four neonatal rabbits within 7 days after birth were randomly divided into sham (n = 8), moderate TAC (50% constriction, n = 8) and severe TAC (sTAC; 75% constriction, n = 8) groups. After the procedure transthoracic echocardiography was performed at 2, 4, and 6 weeks to measure left ventricle structure and function. Histologic staining and gene sequencing of left ventricle myocardial tissue were performed at 6 weeks.Six weeks after procedure transthoracic echocardiography showed that the pressure at the ligation of the aorta was 12.13 ± 0.95 mm Hg in the sTAC group, which was 26 times more than that of the sham group (P.05), and left ventricular dilatation began to appear in the sTAC group. Gene sequencing showed significantly different microRNA expression between the sTAC and sham groups. Bioinformatics analysis among the 3 groups showed that the expression of ocu-miR-411-5p, ocu-miR-214-3p, and ocu-miR-432-5p was decreased in the sTAC group compared with the sham group (P.05) and that the focal adhesion, insulin, and PI3K-Akt signaling pathways were also affected.Aortic constriction of 75% was optimal for the establishment of the PHF model. The expression of ocu-miR-411-5p, ocu-miR-214-3p, and ocu-miR-432-5p was significantly decreased, and the focal adhesion, insulin, and PI3K/AKT pathways may play significant roles in PHF progression.
