Horm Metab Res 2009; 41(2): 152-158
DOI: 10.1055/s-0028-1086023

© Georg Thieme Verlag KG Stuttgart · New York

NAD(P)H Oxidase and Endothelial Dysfunction

G. Muller 1 , H. Morawietz 1
  • 1Division of Vascular Endothelium and Microcirculation, Department of Medicine III, University of Technology Dresden, Dresden, Germany
Further Information

Publication History

received 03.06.2008

accepted 12.08.2008

Publication Date:
24 September 2008 (online)


The regulation of endothelial function plays an important role in the development and progression of metabolic and cardiovascular diseases. A critical determinant of endothelial function is the balance between nitric oxide and reactive oxygen species. Endothelium-derived NO availability can be limited by enhanced formation of reactive oxygen species. Major sources of reactive oxygen species in the vessel wall are NAD(P)H oxidase complexes. This review summarizes the impact of vascular NAD(P)H oxidase-derived reactive oxygen species on atherosclerosis and endothelial dysfunction. Changes in NAD(P)H oxidase expression and activity have clinical implications. Mutations in NAD(P)H oxidase subunits can lead to impaired oxidative burst in leukocytes and chronic granulomatous disease. In contrast, normalization of increased expression and activity of NAD(P)H oxidase in endothelial dysfunction and vascular disorders can be considered as a novel therapeutic strategy in the treatment of cardiovascular diseases.



H. Morawietz, PhD 

Division of Vascular Endothelium and Microcirculation

Department of Medicine III

Carl Gustav Carus Medical School

University of Technology Dresden

Fetscherstraße 74

01307 Dresden


Phone: +49/351/458 66 25

Fax: +49/351/458 63 54

Email: [email protected]