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氧化应激:心房颤动的一种可能发病机制。

Oxidative stress: a possible pathogenesis of atrial fibrillation.

作者信息

Huang Cong-Xin, Liu Yu, Xia Wen-Fang, Tang Yan-Hong, Huang He

机构信息

Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China.

出版信息

Med Hypotheses. 2009 Apr;72(4):466-7. doi: 10.1016/j.mehy.2008.08.031. Epub 2008 Dec 21.

DOI:10.1016/j.mehy.2008.08.031
PMID:19103473
Abstract

Atrial fibrillation (AF) is the most commonly sustained arrhythmia in clinical practice. Despite the extensive studies, the pathophysiology of AF, however, remains incompletely understood. Studies have demonstrated that oxidative stress may be involved in cardiac structural and electrical remodeling. More recently, a growing body of evidence suggests that oxidative stress is associated with the development of AF. The evidence for the hypotheses included that: (1) histological studies have demonstrated oxidative damage in both AF patients and animal models of AF; (2) oxidative stress markers are increased in AF patients, and are associated with the presence of AF; (3) drugs that have antioxidant properties show beneficial effects on AF development. Although the studies suggest the association between oxidative stress and AF, the exact pathogenesis of oxidative stress in AF development remains elusive and requires further investigation. Specifically, the causality between oxidative stress and AF; the levels of the oxidative stress in various types of AFs and their role in the pathogenesis of AF; the effects of strategies to reduce oxidative stress on atrial structural and electrical remodeling, and their exact role in the development of AF. Oxidative stress may provide a scientific basis for further research on the underlying mechanisms of AF and may target for pharmacological interruption of AF.

摘要

心房颤动(AF)是临床实践中最常见的持续性心律失常。尽管进行了广泛的研究,但AF的病理生理学仍未完全了解。研究表明,氧化应激可能参与心脏结构和电重构。最近,越来越多的证据表明氧化应激与AF的发生有关。该假说的证据包括:(1)组织学研究已证实AF患者和AF动物模型中均存在氧化损伤;(2)AF患者的氧化应激标志物升高,且与AF的存在相关;(3)具有抗氧化特性的药物对AF的发生具有有益作用。尽管这些研究表明氧化应激与AF之间存在关联,但氧化应激在AF发生的确切发病机制仍不清楚,需要进一步研究。具体而言,氧化应激与AF之间的因果关系;各种类型AF中氧化应激的水平及其在AF发病机制中的作用;降低氧化应激的策略对心房结构和电重构的影响,以及它们在AF发生中的确切作用。氧化应激可能为进一步研究AF的潜在机制提供科学依据,并可能成为AF药物阻断的靶点。

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