Abstract: Objective: To explore the influences of long non-coding RNA miR-22 host gene (lncRNA MIR-22HG) on cardiomyocyte apoptosis and ventricular remodeling in mice with acute myocardial infarction (AMI) by regulating miR-132-3p/Toll-like receptor 2 (TLR2) axis.Methods: C57BL/6J mice were randomly grouped into sham group, AMI group, AMI+sh-NC group, AMI+sh-MIR22HG group, AMI+sh-MIR22HG+antagomir-NC group, and AMI+sh-MIR22HG+antagomir-132-3p group, with 10 in each group.Except that the sham group only underwent thoracotomy without coronary artery ligation, all the other groups underwent ligation of the left anterior descending coronary artery.Among them, mice in the AMI+sh-NC group, AMI+sh-MIR22HG group, AMI+sh-MIR22HG+antagomir-NC group, and AMI+sh-MIR22HG+antagomir-132-3p group were injected with sh-NC, sh-MIR22HG, sh-MIR22HG+antagomir-NC, and sh-MIR22HG+antagomir-132-3p corresponding to the tail vein, respectively.Echocardiography was used to assess ventricular remodeling and cardiac function in mice; HE staining and Masson staining were applied to observe myocardial histopathological changes and fibrosis; real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was applied to detect the expressions of MIR22HG and miR-132-3p in myocardial tissue; TUNEL method was applied to detect cardiomyocyte apoptosis; western blotting was applied to detect the expressions of myocardial tissue B-cell lymphoma-2 (Bcl-2), activated cysteine protease-3 (cleved caspase-3)/cysteine protease-3 (caspase-3), type Ⅰ collagen (collagen Ⅰ) I, collagen Ⅲ and α-smooth muscle actin (α-SMA); and dual-luciferase reporter assays were applied to verify the relationship between MIR22HG and miR-132-3p, miR-132-3p and TLR2, respectively.Results: Compared with the sham group, the cardiac function of the mice in the AMI group obviously decreased, and myocardial tissue damage and myocardial fibrosis were aggravated.The cardiomyocyte apoptosis rate, the expressions of MIR22HG, TLR2, cleved caspase-3/caspase-3, collagen Ⅰ, collagen Ⅲ and α-SMA proteins obviously increased, while the protein expressions of miR-132-3p and Bcl-2 decreased (P< 0.05).Compared with the AMI+sh-NC group, the cardiac function of the mice in the AMI+sh-MIR22HG group was obviously improved, and myocardial tissue damage and myocardial fibrosis were alleviated; the cardiomyocyte apoptosis rate, the expressions of MIR22HG, TLR2, cleved caspase-3/caspase-3, collagenⅠ, collagen Ⅲ and α-SMA proteins obviously decreased, while the protein expressions of miR-132-3p and Bcl-2 increased (P< 0.05); down-regulation of miR-132-3p attenuated the protective effect of knockdown of MIR22HG on myocardial tissue; the results of the dual-luciferase reporter gene assay showed that MIR22HG targeting regulated the expression of miR-132-3p, and miR-132-3p targeting negatively regulated the expression of TLR2.Conclusion: Inhibition of MIR22HG expression can inhibit cardiomyocyte apoptosis and improve ventricular remodeling in AMI mice by regulating the miR-132-3p/TLR2 axis.