Cardiac　hypertrophy　is　an　independent　predictor　of　cardiovascular　morbidity　and　mortality.　To　identify　the　mechanisms　by　which　simvastatin　inhibits　cardiac　hypertrophy　induced　by　pressure　overload,　we　determined　effects　of　simvastatin　on　14-3-3　protein　expression　and　autophagic　activity.　Simvastatin　was　administered　intragastrically　to　Sprague-Dawley　(SD)　rats　before　abdominal　aortic　banding　(AAB).　Neonatal　rat　cardiomyocytes　(NRCs)　were　treated　with　simvastatin　before　angiotensin　II　(AngII)　stimulation.　14-3-3,　LC3,　and　p62　protein　levels　were　determined　by　western　blot.　Autophagy　was　also　measured　by　the　double-labeled　red　fluorescent　protein-green　fluorescent　protein　autophagy　reporter　system.　Simvastatin　alleviated　excessive　autophagy,　characterized　by　a　high　LC3II/LC3I　ratio　and　low　level　of　p62,　and　blunted　cardiac　hypertrophy　while　increasing　14-3-3　protein　expression　in　rats　that　had　undergone　AAB.　In　addition,　it　increased　14-3-3　expression　and　inhibited　excessive　autophagy　in　NRCs　exposed　to　AngII.　Our　study　demonstrated　that　simvastatin　may　inhibit　excessive　autophagy,　increase　14-3-3　expression,　and　finally　exert　beneficial　effects　on　cardioprotection　against　pressure　overload.