Consistent with the findings of previous studies, our results indicate that, in addition to the direct activation of EndMT/EMT-related proteins, the depletion of Sema3A by TGF-β and miR-181b negatively regulates LIMK/p-cofilin signaling and facilitates actin remodeling and reorganization, which are among the essential molecular processes of EndMT in AF. This evidence concerns the gene TGFB1 and atrial fibrillation.