SMAD2 and renal fibrosis: Das et al. found that the expression of NOX4 caused by TGF-β activation can be reduced by blocking Smad2 or Smad3, which suggested that TGF-β/Smad2/3 upregulated NOX4 and induced ROS generation, such as H2O2, which played an important role in the progression of renal fibrosis [76–78].