Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis
Authors: Louis J Ignarro
Claudio Napoli
Journal: Current Diabetes Reports (2005)
Discipline: CLINICAL MEDICINE
Keywords: nitric oxide; endothelial nitric oxide synthase; atherosclerosis; unstable atheroma; endothelial damage
Affiliations: Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, 23-305 Center for Health Sciences, Los Angeles, CA 90095, USA. 

Abstract:  There is a complex pathophysiologic scenario involving nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and the development of atherosclerosis and unstable atheroma. Endothelial damage induced by atherosclerosis leads to the reduction in bioactivity of eNOS with subsequent impaired release of NO. An important mechanism is local enhanced degradation of NO by increased generation of reactive oxygen species and other free radicals, with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Novel molecular approaches have resulted in the development of new strains of mice lacking eNOS. These experimental models will help to understand how to implement NO-based therapies against atherosclerosis. L-arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. The target or goal for new drugs should be the complete restoration of NO-mediated signaling pathways in atherosclerotic arteries. 

Retracted: No

PubPeer comments:
 2 closely spaced reviews very similar. Review. Curr Diab Rep . 2005 Feb;5(1):17-23. doi: 10.1007 s11892-005-0062-8. Novel Features of Nitric Oxide, Endothelial Nitric Oxide Synthase, and Atherosclerosis Louis J Ignarro 1, Claudio Napoli Affiliation 1Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, 23-305 Center for Health Sciences, Los Angeles, CA 90095, USA. lignarro@mednet.ucla.edu PMID: 15663912 DOI: 10.1007 s11892-005-0062-8 Abstract There is a complex pathophysiologic scenario involving nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and the development of atherosclerosis and unstable atheroma. Endothelial damage induced by atherosclerosis leads to the reduction in bioactivity of eNOS with subsequent impaired release of NO. An important mechanism is local enhanced degradation of NO by increased generation of reactive oxygen species and other free radicals, with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Novel molecular approaches have resulted in the development of new strains of mice lacking eNOS. These experimental models will help to understand how to implement NO-based therapies against atherosclerosis. L-arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. The target or goal for new drugs should be the complete restoration of NO-mediated signaling pathways in atherosclerotic arteries. Review. Curr Atheroscler Rep. 2004 Jul;6(4):281-7. doi: 10.1007 s11883-004-0059-9. Novel Features of Nitric Oxide, Endothelial Nitric Oxide Synthase, and Atherosclerosis Louis J Ignarro 1, Claudio Napoli Affiliation 1Department of Molecular and Medical Pharmacology, David Geffen School of Medicine, University of California, 12-138 Center for Health Sciences, Los Angeles, CA 90095, USA. lignarro@mednet.ucla.edu PMID: 15191702 DOI: 10.1007 s11883-004-0059-9 Abstract There is a complex pathophysiologic scenario involving nitric oxide (NO), endothelial nitric oxide synthase (eNOS), and the development of atherosclerosis and unstable atheroma. Endothelial damage induced by atherosclerosis leads to the reduction in bioactivity of ENOS with subsequent impaired release of NO. An important mechanism is local enhanced degradation of NO by increased generation of reactive oxygen species and other free radicals, with subsequent cascade of oxidation-sensitive mechanisms in the arterial wall. Novel molecular approaches have resulted in the development of new strains of mice lacking eNOS. These experimental models will help to understand how to implement NO-based therapies against atherosclerosis. L-arginine, the precursor of NO, has demonstrated beneficial effects in atherosclerosis and disturbed shear stress. The target or goal for new drugs should be the complete restoration of NO-mediated signaling pathways in atherosclerotic arteries. ,