【Objective】To investigate the role and the potential target of miR-92b-3p in angiotensin Ⅱ（Ang-Ⅱ）-induced mouse cardiac hypertrophy. 【Methods】Ang- Ⅱ- induced cardiac hypertrophy models were established in adult C57BL/6 mice. AgomiR-92b-3p，the cholesterol-modified miR-92b-3p mimic，was delivered to increase the level of miR-92b-3p in mouse myocar? dium via tail vein injection. In the present study，three groups of mice were used in the animal experiment as follows，the agomiR- negative control （agomiR-NC）+saline group，the agomiR-NC+Ang-Ⅱ group and the agomiR-92b-3p+Ang-Ⅱ group. A cell model of cardiac hypertrophy was also established in Ang-Ⅱ-induced neonatal mouse cardiomyocytes in this study Luciferase activity was assayed after transfection using a luciferase reporter assay system. The expression of Myocyte-specific enhancer factor 2D（MEF2D） and hypertrophy-related genes atrial natriuretic peptide（ANP），cardiac muscle α-actin（ACTA1）and β-myosin heavy chain （MHC）at mRNA and protein levels in Ang-Ⅱ-induced hypertrophic myocardium and cardiomyocytes were detected by qRT-PCR and Western blot，respectively.【Results】The expression of ANP，ACTA1，β-MHC were markedly increased in Ang-Ⅱ-induced hypertrophic myocardium and cardiomyocytes. Dual luciferase reporter assay revealed that MEF2D is a potential target gene of miR-92b-3p. And miR-92b-3p can reduce the expression of MEF2D at the post-transcriptional level. Functionally，miR-92b-3p mimic， consistent with MEF2D siRNA，inhibited cell size increase and protein expression of ANP，ACTA1 and β-MHC in Ang-II-treated mouse cardiomyocytes.【Conclusions】MEF2D is a novel target of miR-92b-3p，a target gene of miR-92b-3，which mediates the ef? fect of miR-92b-3p on attenuating cardiomyocyte hypertrophy.