Vascular NAD(P)H oxidases: specific features, expression, and regulation
- PMID: 12855411
- DOI: 10.1152/ajpregu.00758.2002
Vascular NAD(P)H oxidases: specific features, expression, and regulation
Abstract
The importance of reactive oxygen species (ROS) in vascular physiology and pathology is becoming increasingly evident. All cell types in the vascular wall produce ROS derived from superoxide-generating protein complexes similar to the leukocyte NADPH oxidase. Specific features of the vascular enzymes include constitutive and inducible activities, substrate specificity, and intracellular superoxide production. Most phagocyte enzyme subunits are found in vascular cells, including the catalytic gp91phox (aka, nox2), which was the earliest member of the newly discovered nox family. However, smooth muscle frequently expresses nox1 rather than gp91phox, and nox4 is additionally present in all cell types. In cell culture, agonists increase ROS production by activating multiple signals, including protein kinase C and Rac, and by upregulating oxidase subunits. The oxidases are also upregulated in vascular disease and are involved in the development of atherosclerosis and a significant part of angiotensin II-induced hypertension, possibly via nox1 and nox4. Likewise, enhanced vascular oxidase activity is associated with diabetes. Therefore, members of this enzyme family appear to be important in vascular biology and disease and constitute promising targets for future therapeutic interventions.
Similar articles
-
Upregulation of the vascular NAD(P)H-oxidase isoforms Nox1 and Nox4 by the renin-angiotensin system in vitro and in vivo.Free Radic Biol Med. 2001 Dec 1;31(11):1456-64. doi: 10.1016/s0891-5849(01)00727-4. Free Radic Biol Med. 2001. PMID: 11728818
-
Novel isoforms of NADPH oxidase in vascular physiology and pathophysiology.Clin Exp Pharmacol Physiol. 2003 Nov;30(11):849-54. doi: 10.1046/j.1440-1681.2003.03929.x. Clin Exp Pharmacol Physiol. 2003. PMID: 14678249 Review.
-
Increased expression of gp91phox homologues of NAD(P)H oxidase in the aortic media during chronic hypertension: involvement of the renin-angiotensin system.Hypertens Res. 2006 Oct;29(10):813-20. doi: 10.1291/hypres.29.813. Hypertens Res. 2006. PMID: 17283869
-
Novel gp91(phox) homologues in vascular smooth muscle cells : nox1 mediates angiotensin II-induced superoxide formation and redox-sensitive signaling pathways.Circ Res. 2001 May 11;88(9):888-94. doi: 10.1161/hh0901.090299. Circ Res. 2001. PMID: 11348997
-
NADPH oxidases in vascular pathology.Antioxid Redox Signal. 2014 Jun 10;20(17):2794-814. doi: 10.1089/ars.2013.5607. Epub 2013 Nov 1. Antioxid Redox Signal. 2014. PMID: 24180474 Free PMC article. Review.
Cited by
-
(Pro)renin receptor mediates both angiotensin II-dependent and -independent oxidative stress in neuronal cells.PLoS One. 2013;8(3):e58339. doi: 10.1371/journal.pone.0058339. Epub 2013 Mar 14. PLoS One. 2013. PMID: 23516464 Free PMC article.
-
Upstream regulators and downstream effectors of NADPH oxidases as novel therapeutic targets for diabetic kidney disease.Mol Cells. 2015 Apr;38(4):285-96. doi: 10.14348/molcells.2015.0010. Epub 2015 Mar 31. Mol Cells. 2015. PMID: 25824546 Free PMC article. Review.
-
MEF2B-Nox1 signaling is critical for stretch-induced phenotypic modulation of vascular smooth muscle cells.Arterioscler Thromb Vasc Biol. 2015 Feb;35(2):430-8. doi: 10.1161/ATVBAHA.114.304936. Epub 2014 Dec 30. Arterioscler Thromb Vasc Biol. 2015. PMID: 25550204 Free PMC article.
-
Diabetes alters activation and repression of pro- and anti-inflammatory signaling pathways in the vasculature.Front Endocrinol (Lausanne). 2013 Jun 5;4:68. doi: 10.3389/fendo.2013.00068. eCollection 2013. Front Endocrinol (Lausanne). 2013. PMID: 23761786 Free PMC article.
-
Vascular oxidative stress: the common link in hypertensive and diabetic vascular disease.J Cardiovasc Pharmacol. 2010 Apr;55(4):308-16. doi: 10.1097/fjc.0b013e3181d89670. J Cardiovasc Pharmacol. 2010. PMID: 20422735 Free PMC article. Review.
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Other Literature Sources
Miscellaneous