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.
| Original language | English |
|---|---|
| Pages (from-to) | 281-287 |
| Number of pages | 7 |
| Journal | Current Atherosclerosis Reports |
| Volume | 6 |
| Issue number | 4 |
| Publication status | Published - Jul 2004 |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
Cite this
Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis. / Ignarro, Louis J.; Napoli, Claudio.
In: Current Atherosclerosis Reports, Vol. 6, No. 4, 07.2004, p. 281-287.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Novel features of nitric oxide, endothelial nitric oxide synthase, and atherosclerosis
AU - Ignarro, Louis J.
AU - Napoli, Claudio
PY - 2004/7
Y1 - 2004/7
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=5444239280&partnerID=8YFLogxK
M3 - Article
VL - 6
SP - 281
EP - 287
JO - Current Atherosclerosis Reports
JF - Current Atherosclerosis Reports
SN - 1523-3804
IS - 4
ER -