ACTA1 and infarction: Our findings revealed that co-transfection with TGFBR1 offset miR-130a’s inhibitory potency on α-SMA and Col-1 in CFs, consistent with one study’s revelation that the application of a TGFBR1 inhibitor reversed CFs differentiation [33]; this report, combined with our results, suggests that miR-130a obstructs CF conversion to myofibroblasts and collagen deposition through miR-130a’s targeting of TGFBR1.In conclusion, we conclude that miR-130a plays an important role in the post-infarction fibrosis process.