Objective To explore the mechanism of exosomal miR ⁃ 130 in mouse atrial myocytes in the pathogenesis of atrial fibrillation（AF）. Methods Following Ang Ⅱ treatment，mouse atrial myocytes were trans⁃ fected with miR⁃130 shRNA lentivirus（sh⁃miR⁃130）or control（sh⁃Crtl）. Exosomes were isolated from the treated atrial myocytes and then co ⁃cultured with THP ⁃ 1 macrophages. Flow cytometry was performed to examine the percentages of CD86⁃ and CD163⁃positive macrophages. In addition，by constructing a transverse aortic arch coarc⁃ tation（TAC）mouse model and injecting sh⁃miR⁃130 into mice to knock down miR⁃130 expression，the role of miR⁃130 in cardiac fibrosis and macrophages polarization in vivo was further studied. Results The expression of miR⁃130 was increased in AngⅡ⁃treated atrial myocyte⁃derived exosomes（AngII⁃Exo）. By transferring miR⁃130， AngⅡ⁃Exo induced M1 polarization in macrophages. TAC mice with or without sh⁃Ctrl control treatment had signifi⁃ cantly higher levels of miR⁃130，whereas TAC mice with sh⁃miR⁃130 injection had significantly lower levels. sh⁃miR⁃130 significantly improved cardiac structure and reduced myocardial size and fibrosis levels in TAC mice. In addition，iNOS + /CD68 + macrophages had significantly decreased while CD163 + /CD68 + macrophages had signifi⁃ cantly increased in left atrial tissue of TAC mice after sh⁃miR⁃130 treatment. Conclusion Exosomes from AngⅡ⁃ treated atrial myocytes have higher levels of miR⁃130 expression，and exosomes promote M1 macrophage polariza⁃ tion by transferring miR⁃130.