Response to Comment on: Thallas-Bonke et al. (2008) Inhibition of NADPH Oxidase Prevents Advanced Glycation End Product–Mediated Damage in Diabetic Nephropathy Through a Protein Kinase C-α–Dependent Pathway: Diabetes 57:460–469, 2008
- 1Juvenile Diabetes Research Foundation (JDRF) Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Medical Research Institute, Melbourne, Victoria, Australia
- 2Department of Medicine and Immunology, Monash University, Alfred Medical Research and Education Precinct, Melbourne, Victoria, Australia
- Corresponding author: Vicki Thallas-Bonke, JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Medical Research Institute, P.O. Box 6492, St. Kilda Rd., Central, Melbourne, Victoria, Australia, 8008. Email: vicki.thallas{at}baker.edu.au
We thank Dr. Yamagishi for his constructive comments (1) on our recent article (2). In response, we agree that it is possible for protein kinase C–α (PKC-α) to be a downstream signaling molecule of NADPH oxidase, further validating this PKC isoform as an important therapeutic target for the treatment of progressive diabetic nephropathy. In the schema of Fig. 7 in our recent …
