TGFB1 and pulmonary fibrosis: Nevertheless, in vitro studies confirmed that ROS demonstrate a pivotal role in TGF-β-induced EMT, through the activation of MAPK (non-Smad) pathways in renal epithelial cells, leading to renal interstitial fibrosis [174], and that pharmacological inhibition of ROS generation and inactivation of PI3K/Akt and MAPK pathways alleviate TGF-β1-induced EMT in bronchial epithelial cells, resulting in minimized pulmonary fibrosis [175].