Reactive oxygen species and oxidative stress

Hyunjin Noh, Hunjoo Ha

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

30 Scopus citations

Abstract

Oxidative stress defined as an excessive production of reactive oxygen species (ROS) surpassing existing antioxidative defense mechanisms plays a critical role in the development and progression of diabetic vascular complications including nephropathy. Over production of ROS in diabetic milieu is both a direct consequence of hyperglycemia and an indirect consequence through advanced glycation end products (AGEs) or mediators of glucotoxicity such as cytokines and growth factors. Among many pathways, nicotinamide adenosine dinucleotide phosphate (NADPH) oxidase and mitochondrial dysfunction have been recognized as two major sources of ROS generation in diabetic kidneys, and NADPH oxidase-derived ROS has been shown to facilitate renal mitochondrial superoxide production in hyperglycemia. Low antioxidant bioavailability promotes cellular oxidative stress leading to additional cellular damage. Although large-scale clinical trials using classical antioxidants have failed to show a significant effect on the development of vascular complications in diabetes, new strategies targeting NF-E2-related factor 2, the primary transcription factor that controls the antioxidant response, mitochondrial dysfunction, or NADPH oxidase might provide a potential approach for the prevention and treatment of diabetic nephropathy.

Original languageEnglish
Title of host publicationDiabetes and The Kidney
EditorsKar Neng Lai, Sydney Tang
Pages102-112
Number of pages11
DOIs
StatePublished - Jun 2011

Publication series

NameContributions to Nephrology
Volume170
ISSN (Print)0302-5144

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