Since the first demonstration of Nox enzyme expression in the kidney in the early 1990s and the subsequent identification of Nox4, or RENOX, a decade later, it has become apparent that the Nox family of reactive oxygen species (ROS) generating enzymes plays an integral role in the normal physiological function of the kidney. As our knowledge of Nox expression patterns and functions in various structures and specialized cell types within the kidney grows, so does the realization that Nox-derived oxidative stress contributes significantly to a wide variety of renal pathologies through their ability to modify lipids and proteins, damage DNA and activate transcriptional programmes. Diverse studies demonstrate key roles for Nox-derived ROS in kidney fibrosis, particularly in settings of chronic renal disease such as diabetic nephropathy. As the most abundant Nox family member in the kidney, much emphasis has been placed on the role of Nox4 in this setting. However, an ever growing body of work continues to uncover key roles for other Nox family members, not only in diabetic kidney disease, but in a diverse array of renal pathological conditions. The objective of the present review is to highlight the latest novel developments in renal Nox biology with an emphasis not only on diabetic nephropathy but many of the other renal disease contexts where oxidative stress is implicated.
Review Article| December 23 2014
Nox and renal disease
Chet E. Holterman;
Naomi C. Read;
Chris R. J. Kennedy
*Department of Medicine, Division of Nephrology, Kidney Research Centre, Ottawa Hospital Research Institute, Ottawa, Canada
†Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Canada
Correspondence: Dr Christopher R.J. Kennedy (email email@example.com).
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Chet E. Holterman, Naomi C. Read, Chris R. J. Kennedy; Nox and renal disease. Clin Sci (Lond) 1 April 2015; 128 (8): 465–481. doi: https://doi.org/10.1042/CS20140361
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