Abstract: Objective To establish a heart failure (HF) cell model and to investigate the role of euchromatic histone-lysine N-methyltransferase 2 (G9a) in the progression of HF by regulating the expression of brain-derived neurotrophic factor （BDNF） through H3K9me2 in cardiomyocytes of H9C2 rats. 
Methods H9C2 rat cardiomyocytes were cultured, passed, gene transfected and oxygen glucose deprivation (OGD)-treated to establish the HF cell model. RT-qPCR and Western blot were used to detect the expression of G9a mRNA in the OGD-treated HF cell model and control group. The expression of BDNF mRNA in OGD-treated HF cell model after G9a knockout was detected. The expression of OGD-treated H9C2 and OGD-treated H3K9me2 after G9a knockout was detected in H9C2 cells. 
Results The expression of G9a was up-regulated in OGD-treated cell models. The apoptosis and injury of H9C2 rat cardiomyocytes after OGD treatment were inhibited by G9a gene deletion. Silencing G9a promoted the expression of BDNF by inhibiting H3K9me2 modification of BDNF promoter. Silencing BDNF partially reversed sh-G9a by activating the TrkB signaling pathway to reduce cardiomyocyte apoptosis and damage. 
Conclusion In HF model of H9C2 rat cardiomyocytes, G9a regulates the expression of BDNF through H3K9me2, and is involved in the development of HF, which can provide ideas for clinical research on HF markers.

Key words: heart failure, brain-derived neurotrophic factor, G9a