In conclusion, this study revealed that hsa-miR-4443 is a key factor in the pathogenesis of AF (40), where it inhibited cell proliferation, migration, invasion, and myofibroblast phenotypic transformation in HCFBs while promoting apoptosis by directly regulating THBS1 expression and inactivating the downstream pathway TGF-β1/Smad. This evidence concerns the gene THBS1 and atrial fibrillation.