AIM: Micro RNAs( mi RNAs) were recognized to play significant roles in cardiac hypertrophy. But,it remains unknown whether cyclin / Rb pathway is modulated by mi RNAs during cardiac hypertrophy. This study investigates the potential roles of micro RNA-1(mi R-1) and micro RNA-16(mi R-16) in modulating cyclin/Rb pathway during cardiomyocyte hypertrophy. METHODS: An animal model of hypertrophy was established in a rat with abdominal aortic constriction( AAC). In addition,a cell model of hypertrophy was also achieved based on PE-promoted neonatal rat ventricular cardiomyocyte. RESULTS: mi R-1 and-16 expression were markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats. Overexpression of mi R-1 and-16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes. Expression of cyclins D1,D2 and E1,CDK6 and phosphorylated p Rb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes,but could be reversed by enforced expression of mi R-1 and-16. CDK6 was validated to be modulated post-transcriptionally by mi R-1,and cyclins D1,D2 and E1 were further validated to be modulated post-transcriptionally by mi R-16. CONCLUSION: Attenuations of mi R-1 and-16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1,D2,E1 and CDK6,and activating cyclin / Rb pathway. This study investigates the potential roles of micro RNA-1 (mi) R-1) and microRNA-16 (mi R-16) in modulating cyclin / Rb pathway during cardiomyocyte hypertrophy. METHODS: An animal model of hypertrophy was established in a rat with abdominal aortic constriction (AAC). model of hypertrophy was also achieved on PE-promoted neonatal rat ventricular cardiomyocyte. RESULTS: mi R-1 and-16 expression were markedly decreased in hypertrophic myocardium and hypertrophic cardiomyocytes in rats. Overexpression of mi R-1 and -16 suppressed rat cardiac hypertrophy and hypertrophic phenotype of cultured cardiomyocytes. Expression of cyclins D1, D2 and E1, CDK6 and phosphorylated p Rb was increased in hypertrophic myocardium and hypertrophic cardiomyocytes, but could be reversedized by enforced e Xpression of mi R-1 and-16. CDK6 was validated to be modulated post-transcriptionally by mi R-1, and cyclins D1, D2 and E1 were further validated to be modulated post-transcriptionally by mi R-16. CONCLUSION: Attenuations of mi R-1 and-16 provoke cardiomyocyte hypertrophy via derepressing the cyclins D1, D2, E1 and CDK6, and activating cyclin / Rb pathway.