Objective:　To　investigate　the　role　and　mechanism　of　miR-24　in　angiotensin　II　induced　myocardial　fibrosis,　by　miR-24　expression　and　interference　recombinant　lentiviral　transduction　in　primary　cardiac　fibroblasts.　Method:　The　primary　cardiac　fibroblasts　were　stimulated　by　angiotensin　II　to　simulate　in　vitro　myocardial　fibrosis.　Cardiac　fibroblasts　were　transduced　with　previously　constructed　miR-24　expression　interference　recombinant　lentivirus.　Cell　proliferation,　apoptosis　and　gene　expression　levels　of　AGTR-1,　beta-arrestin-1,　GNAQ　and　PKC-delta　were　detected　to　identify　the　target　of　miR-24.　PKC-delta　expression　recombinant　lentivirus　was　constructed　to　investigate　the　effect　of　miR-24　on　AGTR1-Gq-PKC　signaling　pathway.　Results:　MiR-24　facilitated　expression　of　AGTR-1　and　beta-arrestin-1　and　cell　apoptosis,　and　inhibited　cell　proliferation　and　the　synthesis　of　hydroxyproline,　exhibiting　a　negative　synergistic　effect　with　PKC-delta.　Conclusion:　miR-24　negatively　regulated　PKC-delta　by　working　on　AGTR1　and　furthermore　inhibited　myocardial　fibrosis　induced　by　angiotensin　II.