Nox4 as a potential therapeutic target for treatment of uremic toxicity associated to chronic kidney disease

摘要

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.