The same group demonstrated that both TUDCA and 4-PBA normalize blood pressure, reduce cardiomyocyte UPR activity and cardiac fibrosis and restore macrovascular endothelial function via inhibition of transforming growth factor-beta 1 (TGF-β1), confirming a key pathogenic role for ER stress in hypertension [118]. This evidence concerns the gene TGFB1 and hypertensive disorder.