期刊
TRENDS IN CARDIOVASCULAR MEDICINE
卷 24, 期 4, 页码 165-169出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tcm.2013.12.001
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资金
- Ministry of Education, Science, and Culture of Japan
- Japan Heart Foundation Grant for Research on Hypertension and Metabolism
- Grant for Research Foundation for Community Medicine
An imbalance of nitric oxide (NO) and reactive oxygen species (ROS), so-called oxidative stress, may promote endothelial dysfunction, leading to cardiovascular complications. Activation of nicotinamide-adenine dinucleotide phosphate oxidase, xanthine oxidase, cyclooxygenase, and mitochondrial electron transport, inactivation of the antioxidant system, and uncoupling of endothelial NO synthase lead to oxidative stress along with an increase in ROS production and decrease in ROS degradation. Although experimental studies, both in vitro and in vivo, have shown a critical role of oxidative stress in endothelial dysfunction under the condition of excessive oxidative stress, there is little information on whether oxidative stress is really involved in endothelial function in humans. In a clinical setting, we showed an association between oxidative stress and endothelial function, especially in patients with renovascular hypertension as a model of increased oxidative stress and in patients with Gilbert syndrome as a model of decreased oxidative stress, through an increase in the antioxidant property of unconjugated bilirubin. (C) 2014 Elsevier Inc. All rights reserved.
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