DNM1L and bacterial urinary tract infection: UTI improved the renal redox equilibrium and mitochondrial functions in the UTI-treated DN group, as evidenced by significant decreases in mitochondrial ROS, H2O2 and 8-OHdG and mitochondrial fission proteins, including Drp1 and FIS1, while it significantly increased mitochondrial ATP level and mitochondrial ΔΨm.