When the TGF-Beta1/Smad3 signalling pathway is impeded, there has been shown to be a reduction in collagen synthesis in cardiac fibroblasts, a reduction in myocardial fibrosis and the prevention of adverse remodelling in cases of pathological overload or damage to the left ventricle [103, 111–114]. Here, SMAD3 is linked to Myocardial fibrosis.