title: Oxidative stress and advanced glycation in diabetic nephropathy.
abstract: Nephropathy remains a significant cause of morbidity and mortality in the diabetic population and is the leading cause of end-stage renal failure in the Western World. As a result of the diabetic milieu, increased generation of reactive oxygen species (ROS) is thought to play a key role in the progression of diabetic nephropathy. Recent experimental studies have suggested that the receptor for advanced glycation end products (RAGE), which is central to the advanced glycation pathway, may mediate renal structural and functional damage via oxidative stress. This review focuses on how RAGE and subsequent ROS generation play a deleterious role in the diabetic kidney, promoting cross-talk among signaling pathways, ultimately leading to renal dysfunction.
authors.affiliation: JDRF Albert Einstein Centre for Diabetes Complications, Diabetes and Metabolism Division, Baker Heart Research Institute, Melbourne, Victoria, Australia. melinda.coughlan@baker.edu.au
authors.forename: Melinda T
authors.initials: MT
authors.lastname: Coughlan
authors.forename: Amy L
authors.initials: AL
authors.lastname: Mibus
authors.forename: Josephine M
authors.initials: JM
authors.lastname: Forbes
mesh_terms: D003928:Diabetic Nephropathies / Q000201:enzymology / Q000503:physiopathology*; D017127:Glycation End Products, Advanced / Q000502:physiology*; D006801:Humans; D019255:NADPH Oxidases / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000009:adverse effects
chemical_list: D017127:Glycation End Products, Advanced; D017382:Reactive Oxygen Species; D019255:NADPH Oxidases