Recently,microRNAs (miRNAs) have been shown to involve in the process of heart failure.This study aims to investigate the functional role of miR-147b in rat H9c2 cardiomyocytes and explore the underlying molecular mechanisms.Cell viability of H9c2 cells was detected by MTT assay.Cell apoptosis was detected by flow cytometry.Expression of miR-147b and KLF13 mRNA was detected by quantitative real-time PCR.The relationship between miR-147b and KLF13 was verified by dual-luciferase reporter assay.Protein levels were detected by weste blot analysis.It was found that H2O2 inhibited cell viability and promoted cell apoptosis of H9c2 cells in a concentration-dependent manner.MiR-147b overexpression suppressed cell viability and increased apoptosis in H9c2 cells,while knock-down of miR-147b increased cell viability and reduced apoptosis in H2O2-treated H9c2 cells.Luciferase reporter assay and in vitro functional assay showed that KLF13 was a downstream target of miR-147b,and KLF13 knock-down suppressed cell viability and induced apoptosis in H9c2 cells.Enforced expression of KLF13 restored the effects of miR-147b overexpression on cell viability and apoptosis in H9c2 cells.MiR-147b modulated the expression levels of apoptosis-related proteins,and the effects of miR-147b overexpression on apoptosis-related proteins levels were prevented by enforced expression of KLF13 in H9c2 cells.The in vivo experiments showed that miR-147b was up-regulated,and KLF13 was down-regulated in the myocardial tissues from rats with chronic heart failure.Collectively,miR-147b inhibits viability and promotes cell apoptosis by targeting KLF13 in H9c2 cells,which may be associated with the pathogenesis of heart failure.