The upregulations of phosphorylated PKC, NOX4, p47phox and p22phox proteins, membrane translocation of p47phox, activation of Rac1, reduced activities of antioxidises including SOD, CAT and GSH, were proposed as potential cellular mechanisms by which salusin-β induced oxidative stress in the process of AKI. This evidence concerns the gene NCF1 and acute kidney injury.