TGFB1 and Myocardial fibrosis: Excess ROS act directly on cardiomyocytes, destroying myofilament structure and function through the oxidative modification of sulfhydryl groups or the carbonylation of key contractile proteins such as actin and myosin [4]; More importantly, ROS induces myofibroblasts to differentiate into myofibroblasts by activating the TGF-β/Smad signalling pathway, promoting collagen deposition and myocardial fibrosis [5].