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Diabetic neuropathy and oxidative stress

dc.contributor.authorPop-Busui, Rodicaen_US
dc.contributor.authorSima, Anders A. F.en_US
dc.contributor.authorStevens, Martin J.en_US
dc.date.accessioned2007-01-17T15:54:50Z
dc.date.available2007-01-17T15:54:50Z
dc.date.issued2006en_US
dc.identifier.citationPop-Busui, Rodica; Sima, Anders; Stevens, Martin (2006)."Diabetic neuropathy and oxidative stress." Diabetes/Metabolism Research and Reviews 9999(9999): n/a-n/a. <http://hdl.handle.net/2027.42/49300>en_US
dc.identifier.issn1520-7552en_US
dc.identifier.issn1520-7560en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/49300
dc.description.abstractThis review will focus on the impact of hyperglycemia-induced oxidative stress in the development of diabetes-related neural dysfunction. Oxidative stress occurs when the balance between the production of reactive oxygen species (ROS) and the ability of cells or tissues to detoxify the free radicals produced during metabolic activity is tilted in the favor of the former. Although hyperglycemia plays a key role in inducing oxidative stress in the diabetic nerve, the contribution of other factors, such as endoneurial hypoxia, transition metal imbalances, and hyperlipidemia have been also suggested. The possible sources for the overproduction of ROS in diabetes are widespread and include enzymatic pathways, auto-oxidation of glucose, and mitochondrial superoxide production. Increase in oxidative stress has clearly been shown to contribute to the pathology of neural and vascular dysfunction in diabetes. Potential therapies for preventing increased oxidative stress in diabetic nerve dysfunction will be discussed. Copyright © 2006 John Wiley & Sons, Ltd.en_US
dc.format.extent400823 bytes
dc.format.extent3118 bytes
dc.format.mimetypeapplication/pdf
dc.format.mimetypetext/plain
dc.language.isoen_US
dc.publisherJohn Wiley & Sons, Ltd.en_US
dc.subject.otherLife and Medical Sciencesen_US
dc.subject.otherDiabetes and Clinical Endocrinologyen_US
dc.titleDiabetic neuropathy and oxidative stressen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelInternal Medicine and Specialtiesen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, MI, USA ; Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, MI, USA.en_US
dc.contributor.affiliationumDepartment of Internal Medicine, Division of Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, MI, USA ; Department of Internal Medicine, University of Birmingham, UKen_US
dc.contributor.affiliationotherDepartment of Pathology, Wayne State University, Detroit, MI, USAen_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/49300/1/899_ftp.pdfen_US
dc.identifier.doihttp://dx.doi.org/10.1002/dmrr.625en_US
dc.identifier.sourceDiabetes/Metabolism Research and Reviewsen_US
dc.owningcollnameInterdisciplinary and Peer-Reviewed


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