Much evidence indicates that the chronic intra-atrial or intra-ventricular volume overload and the activation of RAAS and SNS resulting from CKD could urge stress relative signaling pathways [e.g., tumor necrosis factor-α, transforming growth factor-β1 (TGF-β1), and NAPDH oxidases, etc.], leading to myocyte apoptosis, interstitial fibrosis and the alteration of electrical activity (8). Here, TGFB1 is linked to chronic kidney disease.