Nitric Oxide and Pathogenic Mechanisms Involved in the Development of Vascular Diseases

被引:234
作者
Napoli, Claudio [1 ,2 ]
Ignarro, Louis J. [3 ,4 ]
机构
[1] Univ Naples 2, Dept Gen Pathol, Sch Med 1, I-80138 Naples, Italy
[2] Univ Naples 2, Excellence Res Ctr Cardiovasc Dis, Sch Med 1, Chair Clin Pathol, I-80138 Naples, Italy
[3] Univ Calif Los Angeles, David Geffen Sch Med, Dept Med & Mol Pharmacol, Ctr Hlth Sci, Los Angeles, CA 90095 USA
[4] Konkuk Univ, Sch Med, WCU Program, Seoul 143701, South Korea
关键词
Nitric oxide; Atherosclerosis; Smooth muscle cells; OXIDATION-SENSITIVE MECHANISMS; KRUPPEL-LIKE FACTOR-2; ENDOTHELIAL-CELLS; EXTRACRANIAL ARTERIES; SYNTHASE EXPRESSION; SHEAR-STRESS; KLF2; ATHEROSCLEROSIS; TRANSCRIPTION; DYSFUNCTION;
D O I
10.1007/s12272-009-1801-1
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Nitric oxide (NO) is a pivotal signaling messenger in the cardiovascular system. NO participates in regulatory functions including control of hemostasis, fibrinolysis, platelet and leukocyte interactions with the arterial wall, regulation of vascular tone, proliferation of vascular smooth muscle cells, and homeostasis of blood pressure. Diminished NO bioavailability and abnormalities in NO-dependent signaling are among central factors of vascular disease, although it is unclear whether this is a cause of, or result of endothelial dysfunction or both pathogenic events. Disturbances in NO bioavailability have been linked to cause endothelial dysfunction, leading to increased susceptibility to atherosclerotic lesion progression, hypertension, hypercholesterolemia, diabetes mellitus, thrombosis and stroke.
引用
收藏
页码:1103 / 1108
页数:6
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