Document Detail


Nox as a target for diabetic complications.
MedLine Citation:
PMID:  23767990     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxidative stress has been linked to the pathogenesis of the major complications of diabetes in the kidney, the heart, the eye or the vasculature. NADPH oxidases of the Nox family are a major source of ROS (reactive oxygen species) and are critical mediators of redox signalling in cells from different organs afflicted by the diabetic milieu. In the present review, we provide an overview of the current knowledge related to the understanding of the role of Nox in the processes that control cell injury induced by hyperglycaemia and other predominant factors enhanced in diabetes, including the renin-angiotensin system, TGF-β (transforming growth factor-β) and AGEs (advanced glycation end-products). These observations support a critical role for Nox homologues in diabetic complications and indicate that NADPH oxidases are an important therapeutic target. Therefore the design and development of small-molecule inhibitors that selectively block Nox oxidases appears to be a reasonable approach to prevent or retard the complications of diabetes in target organs. The bioefficacy of these agents in experimental animal models is also discussed in the present review.
Authors:
Yves Gorin; Karen Block
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Review    
Journal Detail:
Title:  Clinical science (London, England : 1979)     Volume:  125     ISSN:  1470-8736     ISO Abbreviation:  Clin. Sci.     Publication Date:  2013 Oct 
Date Detail:
Created Date:  2013-06-17     Completed Date:  2013-08-28     Revised Date:  2014-05-02    
Medline Journal Info:
Nlm Unique ID:  7905731     Medline TA:  Clin Sci (Lond)     Country:  England    
Other Details:
Languages:  eng     Pagination:  361-82     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Diabetes Complications / metabolism*,  prevention & control
Enzyme Inhibitors / therapeutic use
Glycosylation End Products, Advanced / antagonists & inhibitors,  metabolism
Humans
Hyperglycemia / metabolism,  prevention & control
NADPH Oxidase / antagonists & inhibitors,  metabolism*
Reactive Oxygen Species / antagonists & inhibitors,  metabolism*
Renin-Angiotensin System / drug effects
Transforming Growth Factor beta / antagonists & inhibitors,  metabolism
Grant Support
ID/Acronym/Agency:
R01 CA 131272/CA/NCI NIH HHS; R01 CA131272/CA/NCI NIH HHS; R01 DK 079996/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Glycosylation End Products, Advanced; 0/Reactive Oxygen Species; 0/Transforming Growth Factor beta; EC 1.6.3.-/NOX4 protein, human; EC 1.6.3.1/NADPH Oxidase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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