Abstract: Objective：To investigate the role and mechanism of miR378 on heat shock factor1 (HSF1) in cardiac hypertrophy induced by pressure overload. Methods：C57B/L6 mice were subjected to pressure overload by thoracic aortic banding (TAC). Twodimensional echocardiographic and hemodynamic examinations were performed at two weeks after TAC. In vitro, cardiomyocytes were mechanically stretched for 24 h. PremiR378 or AntimiR378 was transfected into cardiomyocytes for 48 h. The expression of HSF1 protein and miR378 were detected by Western blotting and qRTPCR. Luciferase reporter assay was used to explore the relationship between miR378 and potential target protein HSF1. Results：At two weeks after TAC contructed, the mice showed compensatory cardiac hypertrophy. Western blotting and qRTPCR showed increase of HSF1 and decrease of miR378 in the heart. Overexpression of miR378 significantly suppressed the expression of HSF1 in cardiomyocytes, while inhibition of endogenous miR378 promoted the upregulation of HSF1 greatly. Luciferase reporter assay showed that miR378 can target HSF1 by binding to the 3′UTR sequence of HSF1. Conclusions：In the compensatory phase of cardiac hypertrophy, miR378 could regulate the expression of endogenous HSF1 in myocardium by targeting the 3′UTR of HSF1.