title: Nox4 and diabetic nephropathy: with a friend like this, who needs enemies?
abstract: Oxidative stress has been linked to the pathogenesis of diabetic nephropathy, a complication of diabetes in the kidney. NADPH oxidases of the Nox family are a major source of reactive oxygen species in the diabetic kidney and are critical mediators of redox signaling in glomerular and tubulointerstitial cells exposed to the diabetic milieu. Here, we present an overview of the current understanding of the roles of Nox catalytic and regulatory subunits in the processes that control mesangial cell, podocyte, and tubulointerstitial cell injury induced by hyperglycemia and other predominant factors enhanced in the diabetic milieu, including the renin-angiotensin system and transforming growth factor-β. The role of the Nox isoform Nox4 in the redox processes that alter renal biology in diabetes is highlighted.
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA. Electronic address: gorin@uthscsa.edu.
authors.forename: Yves
authors.initials: Y
authors.lastname: Gorin
authors.affiliation: Department of Medicine, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA; Audie L. Murphy Memorial Hospital Division, South Texas Veterans Health Care System, San Antonio, TX 78229, USA. Electronic address: block@uthscsa.edu.
authors.forename: Karen
authors.initials: K
authors.lastname: Block
mesh_terms: D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000209:etiology* / Q000378:metabolism; D005920:Glomerular Mesangium / Q000473:pathology; D006801:Humans; D007684:Kidney Tubules / Q000473:pathology; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases / Q000037:antagonists & inhibitors / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species; D000074663:NADPH Oxidase 4; D019255:NADPH Oxidases; C498910:NOX4 protein, human
keywords: Diabetic complications; Diabetic nephropathy; Free radicals; Glomerular cell injury; Hyperglycemia; NADPH oxidases of the Nox family; Nox4; Oxidative stress; Reactive oxygen species; Tubulointerstitial cell injury