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心血管损伤中氧化应激和活性氧的基本机制。

Basic mechanisms of oxidative stress and reactive oxygen species in cardiovascular injury.

作者信息

Papaharalambus Christopher A, Griendling Kathy K

机构信息

Division of Cardiology, Department of Medicine, Emory University, Atlanta, GA 30322, USA.

出版信息

Trends Cardiovasc Med. 2007 Feb;17(2):48-54. doi: 10.1016/j.tcm.2006.11.005.

Abstract

The development of vascular disease has its origins in an initial insult to the vessel wall by biological or mechanical factors. The disruption of homeostatic mechanisms leads to alteration of the original architecture of the vessel and its biological responsiveness, contributing to acute or chronic diseases such as stroke, hypertension, and atherosclerosis. Endothelial dysfunction, macrophage infiltration of the vessel wall, and proliferation and migration of smooth muscle cells all involve different types of reactive oxygen species produced by various vessel wall components. Although basic science and animal research have clearly established the role of reactive oxygen species in the progression of vascular disease, the failure of clinical trials with antioxidant compounds has underscored the need for better antioxidant therapies and a more thorough understanding of the role of reactive oxygen species in cardiovascular physiology and pathology.

摘要

血管疾病的发展起源于生物或机械因素对血管壁的初始损伤。稳态机制的破坏导致血管原始结构及其生物反应性的改变,从而引发诸如中风、高血压和动脉粥样硬化等急性或慢性疾病。内皮功能障碍、血管壁巨噬细胞浸润以及平滑肌细胞的增殖和迁移均涉及血管壁各成分产生的不同类型的活性氧。尽管基础科学和动物研究已明确证实活性氧在血管疾病进展中的作用,但抗氧化化合物临床试验的失败凸显了开发更好的抗氧化疗法以及更深入了解活性氧在心血管生理和病理中的作用的必要性。

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