SMAD3 and myocardial infarction: When primary cilium is disrupted in cardiac fibroblasts due to cardiac fibroblast-specific Pkd1 deletion, the TGFβ-Smad3 signaling-induced ECM protein production and myofibroblast differentiation of cardiac fibroblasts were impaired, leading to insufficient scar formation and increased cardiomyocyte hypertrophy after MI (Villalobos et al., 2019).