Copyright © 2004, European Society of Cardiology
Vascular NADPH oxidases: molecular mechanisms of activation
Institut für Kardiovaskuläre Physiologie, Universität Frankfurt, Frankfurt, Germany
Innere Medizin III, Universität Heidelberg, Heidelberg, Germany
* Corresponding author. Institut für Kardiovaskuläre Physiologie, Klinikum der J.W. Goethe-Universität, Theodor-Stern-Kai 7, D-60596 Frankfurt am Main, Germany. Tel.: +49 69 6301 6995; fax: +49 69 6301 7668. Email address: r.brandes{at}em.uni-frankfurt.de
Oxygen-derived free radicals are thought to contribute to the initiation and progression of cardiovascular disease via several different mechanisms, such as consumption of nitric oxide, oxidation of proteins and lipids, and activation of redox-sensitive signalling cascades. Vascular NADPH oxidases are important sources of vascular radical formation. The activities of these enzymes, which in some aspects are similar to the leukocyte NADPH oxidase, are controlled on the expression level and complex activation mechanisms. As a plethora of vascular stimuli, such as growth factors, cytokines, physical stimuli, and lipids elicits radical formation by these enzymes, a careful analysis is required for the understanding of the activation of the NADPH oxidases. This article reviews the components of the NADPH oxidases in leukocytes and vascular tissue. Emphasis is put on the activation of the oxidases, including upstream signalling events and molecular modes of interaction between the subunits.
KEYWORDS NADPH oxidase; p22phox; Oxygen-derived free radicals; Nox
Time for primary review 19 days
![]()
CiteULike
Connotea
Del.icio.us What's this?
This article has been cited by other articles:
![]() |
J. Yatabe, H. Sanada, M. S. Yatabe, S. Hashimoto, M. Yoneda, R. A. Felder, P. A. Jose, and T. Watanabe Angiotensin II type 1 receptor blocker attenuates the activation of ERK and NADPH oxidase by mechanical strain in mesangial cells in the absence of angiotensin II Am J Physiol Renal Physiol, May 1, 2009; 296(5): F1052 - F1060. [Abstract] [Full Text] [PDF] |
||||
![]() |
W. G. Mayhan, D. M. Arrick, G. M. Sharpe, and H. Sun Nitric oxide synthase-dependent responses of the basilar artery during acute infusion of nicotine Nicotine Tob Res, March 1, 2009; 11(3): 270 - 277. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. Zhang, M. Hou, Y. Li, X. Xu, M. Barsoum, Y. Chen, and R. J. Bache NADPH oxidase contributes to coronary endothelial dysfunction in the failing heart Am J Physiol Heart Circ Physiol, March 1, 2009; 296(3): H840 - H846. [Abstract] [Full Text] [PDF] |
||||
![]() |
Z. Wang, T. Rui, M. Yang, F. Valiyeva, and P. R. Kvietys Alveolar Macrophages from Septic Mice Promote Polymorphonuclear Leukocyte Transendothelial Migration via an Endothelial Cell Src Kinase/NADPH Oxidase Pathway J. Immunol., December 15, 2008; 181(12): 8735 - 8744. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Li, X. Dai, S. Watts, D. Kreulen, and G. Fink Increased superoxide levels in ganglia and sympathoexcitation are involved in sarafotoxin 6c-induced hypertension Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2008; 295(5): R1546 - R1554. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Chen, H. Chai, X. Wang, J. Jiang, M. S. Jamaluddin, D. Liao, Y. Zhang, H. Wang, U. Bharadwaj, S. Zhang, et al. Soluble CD40 ligand induces endothelial dysfunction in human and porcine coronary artery endothelial cells Blood, October 15, 2008; 112(8): 3205 - 3216. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. Urbich, A. Kuehbacher, and S. Dimmeler Role of microRNAs in vascular diseases, inflammation, and angiogenesis Cardiovasc Res, September 1, 2008; 79(4): 581 - 588. [Abstract] [Full Text] [PDF] |
||||
![]() |
S. Kumar, X. Sun, S. Wedgwood, and S. M. Black Hydrogen peroxide decreases endothelial nitric oxide synthase promoter activity through the inhibition of AP-1 activity Am J Physiol Lung Cell Mol Physiol, August 1, 2008; 295(2): L370 - L377. [Abstract] [Full Text] [PDF] |
||||
![]() |
P. M. Vanhoutte Arginine and Arginase: Endothelial NO Synthase Double Crossed? Circ. Res., April 25, 2008; 102(8): 866 - 868. [Full Text] [PDF] |
||||








