Objective:To investigate the relationship between miR-23b expression abnormalities and developmental defects of the heart. Methods:Human and developing mouse embryo myocardial tissues were collected. P19 cells,induced to differentiating into cardiomyocytes with 0.9% dimethyl sulfoxide (DMSO),were collected at day 0,4,6,10. MiR-23b expression level of the mentioned tissues or cells was then detected. Online databases were used to predict target genes of miR-23b and the signaling pathways that the target genes may be involved in,thus to comprehensively analyze the relationship between miR-23b expression abnormalities and developmental defects of the heart. Results:For human embryos of first and second trimester of gestation,miR-23b expression was upregulated 4.4 times and downregulated 3.5 times,respectively,in the VSD (ventricular septal defect) group,compared with the normal control group. For mouse embryos,expression of miR-23b increased gradually at the four time points:d12.5,d14.5,d16.5,d18.5. Differences among the later three time points (after d14.5) were significant (P < 0.05). During differentiating into cardiomyocytes,P19 cells showed a descending trend in miR-23b expression. Differences between d4 and d6 or d6 and d10 were significant (P < 0.05). Bioinformatics about miR-23b suggests that it may be involved in TGF-β,Notch,Wnt signaling pathways. Conclusion:MiR-23b expression abnormalities may influence proliferation,apoptosis,migration and differentiation of cardiomyocytes and thus result in developmental defects of the heart.