Mechanistically, BV treatment led to ROS generation and the activation of the Bip/eIF2α/CHOP signaling pathway and subsequently caused ER stress, UPR, and cytoplasmic Ca2+ overloading, both of which in turn regulated the expressions of classical signals involved in EMT and fibrosis, ultimately resulting in renal fibrosis in renal tubular epithelial cells. This evidence concerns the gene DDIT3 and renal fibrosis.