Mitochondria and RAAS-mediated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase as well as activation and expression of pro-inflammatory cytokines are principal sources of cardiac oxidative stress and fibrosis through increased ROS production and activation of TGF-β1/Smad signaling pathway, and contribute to DCM development and progression (Midaoui et al., 2003; Li et al., 2009; Lee et al., 2012; Murdoch et al., 2014; Jia et al., 2016). Here, TGFB1 is linked to familial dilated cardiomyopathy.