The mechanism of the role of ROS in the formation of renal fibrosis can be interpreted as follows: High glucose induces the increased expression of NADPH oxidase 4 (NOX4), contributing to the overproduction of ROS, which activates the TGF-β/Smads pathway and other pro-fibrotic factors (36, 41). This evidence concerns the gene TGFB1 and renal fibrosis.