Cellular and molecular mechanisms of endothelial cell dysfunction
Cellular and molecular mechanisms of endothelial cell dysfunction
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DOI：
10.1172/jci119751
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发表时间：
1997-11-01
影响因子：
15.9
通讯作者：
Harrison, DG
中科院分区：
文献类型：
--
作者：
Harrison, DG
血管L-精氨酸/一氧化氮（NO）1合酶系统与血管生物学的临床相关性在于反复观察到它被各种病理生理条件改变。NO产生和/或生物利用度的这种改变已经显示在实验动物模型和人类受试者中发生，在诸如高血压、高胆固醇血症、衰老、吸烟、糖尿病和心力衰竭的各种疾病的背景下（1）。内皮细胞这一重要功能改变的机制多种多样，可能是多因素的。在过去的几年中，大量的研究致力于了解这些异常，这导致了对血管张力，氧化还原状态，炎症，生长和血管壁的促血栓形成/抗血栓形成特性的调节的新见解。这一观点将突出一些重要的新观察，因为它们涉及到内皮细胞L-精氨酸/NO合酶（NOS）系统的病理。此外，未来的研究方向，可能是特别翔实的将被指出。
The clinical relevance of the vascular L-arginine/nitric oxide (NO) 1 synthase system to vascular biology lies in the oftrepeated observation that it is altered by a variety of pathophysiological conditions. Such alterations of NO production and/or bioavailability have been shown to occur both in experimental animal models and in human subjects, in the setting of such diverse disorders as hypertension, hypercholesterolemia, aging, cigarette smoking, diabetes, and heart failure (1). The mechanisms underlying the alteration of this important function of the endothelium are varied and likely multifactorial. During the past several years an enormous amount of research has been devoted to understanding these abnormalities, which has led to new insights into regulation of vascular tone, redox state, inflammation, growth, and the prothrombotic/antithrombotic properties of the vessel wall. This Perspective will highlight some of these important new observations, as they relate to the pathology of the endothelial cell L-arginine/NO synthase (NOS) system. In addition, future directions of research that may be particularly informative will be indicated.