In a study by Che et al., miR-150-5p inhibited the binding of Smad7 to ALK5 by directly targeting smad7, which promoted the increase of the binding of Smad2/3 to ALK5, thereby promoting the high expression of TGF-β/Smad2/3 signal, accelerating extracellular collagen deposition, and exacerbating the process of myocardial fibrosis (Che et al., 2019). Here, SMAD7 is linked to Myocardial fibrosis.