Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy.

@article{Jha2014GeneticTO,
  title={Genetic targeting or pharmacologic inhibition of NADPH oxidase nox4 provides renoprotection in long-term diabetic nephropathy.},
  author={Jay C. Jha and Stephen P. Gray and David Barit and Jun Okabe and Assam El-Osta and Tamehachi Namikoshi and Vicki Thallas-Bonke and Kirstin Wingler and C{\'e}dric Szyndralewiez and Freddy Heitz and Rhian M Touyz and Mark Emmanuel Cooper and Harald H H W Schmidt and Karin Jandeleit-Dahm},
  journal={Journal of the American Society of Nephrology : JASN},
  year={2014},
  volume={25 6},
  pages={1237-54}
}
Diabetic nephropathy may occur, in part, as a result of intrarenal oxidative stress. NADPH oxidases comprise the only known dedicated reactive oxygen species (ROS)-forming enzyme family. In the rodent kidney, three isoforms of the catalytic subunit of NADPH oxidase are expressed (Nox1, Nox2, and Nox4). Here we show that Nox4 is the main source of renal ROS in a mouse model of diabetic nephropathy induced by streptozotocin administration in ApoE(-/-) mice. Deletion of Nox4, but not of Nox1… CONTINUE READING