title: Oxidative stress and diabetic kidney disease.
abstract: The number of people with diabetic kidney disease continues to increase worldwide despite current treatments. Of the pathophysiologic mechanisms that have been identified in the development and progression of diabetic nephropathy, oxidative stress (more accurately described as increased levels of reactive oxygen species; ROS) is of major importance. The increase in ROS is due to both increased production and to decreased and/or inadequate antioxidant function. To date, human clinical trials with antioxidants have not been shown to be effective. This is likely due, at least in part, to the lack of specificity of current agents. Recent research has determined both major sources of high glucose-induced cellular ROS production as well as high glucose-induced changes in antioxidant function. Treatments targeted at one or more of the specific diabetes-induced alterations in the regulation of ROS levels will likely lead to effective treatments that prevent the development and progression of diabetic kidney disease.
authors.affiliation: Harvard Medical School, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA. robert.stanton@joslin.harvard.edu
authors.forename: Robert C
authors.initials: RC
authors.lastname: Stanton
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000378:metabolism*; D006801:Humans; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species