Abstract
Watanabe et al. report that Nox4 NADPH oxidase catalytic moiety and the subunit p22(phox) mediate the increase in oxidative stress and human tubular epithelial cell injury induced by p-cresyl sulfate, a protein-bound uremic toxin. These findings could be instrumental for the design of novel therapeutic intervention utilizing small-molecule inhibitors specifically targeting Nox oxidases to prevent or slow down the progression of chronic kidney disease and the associated disorders due to uremic toxicity.