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睡眠呼吸障碍与脑血管疾病:一种机制性方法

Sleep-disordered breathing and cerebrovascular disease: a mechanistic approach.

作者信息

Lavie Lena

机构信息

The Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, POB 9649, 31096, Haifa, Israel.

出版信息

Neurol Clin. 2005 Nov;23(4):1059-75. doi: 10.1016/j.ncl.2005.05.005.

Abstract

The observations described in this article point to the existence of increased oxidative stress and systemic inflammation in sleep apnea and have paved the way for establishing sleep apnea as an independent risk factor for cardio- and cerebrovascular morbidities. The proposed course of events is summarized in Fig. 1. It is suggested that hypoxia/reoxygenation,characteristic of sleep apnea, promotes the formation of ROS, particularly during the reoxygenation period, and can be deleterious to cells and tissues. ROS, however, regulate the activation of critical transcription factors that are redox sensitive, resulting in increased expression of sets of genes that encode proteins essential to adaptation to hypoxia (via hypoxia inducible factor I [hypoxia inducible factor-la]). Yet, redox-sensitive transcription factors (NFKB and AP-1) that elicit inflammatory pathways also are activated, thereby affecting inflammatory and immune responses by promoting activation of endothelial cells, leukocytes, and platelets. These activated cells express adhesion molecules and proinflammatory cytokines that may lead to endothelial injury and dysfunction and consequently to the development of cardio- and cerebrovascular morbidities. These may be exaggerated in patients who have sleep apnea in response to the intermittent hypoxia.

摘要

本文所述的观察结果表明,睡眠呼吸暂停患者存在氧化应激增加和全身炎症反应,为将睡眠呼吸暂停确立为心血管和脑血管疾病的独立危险因素铺平了道路。建议的事件过程总结于图1。研究表明,睡眠呼吸暂停的特征性缺氧/复氧过程,特别是在复氧期,会促进活性氧(ROS)的形成,对细胞和组织有害。然而,ROS会调节对氧化还原敏感的关键转录因子的激活,导致编码适应缺氧所必需蛋白质的基因集(通过缺氧诱导因子I [缺氧诱导因子-1α])表达增加。然而,引发炎症途径的氧化还原敏感转录因子(NF-κB和AP-1)也会被激活,从而通过促进内皮细胞、白细胞和血小板的激活来影响炎症和免疫反应。这些活化细胞表达粘附分子和促炎细胞因子,可能导致内皮损伤和功能障碍,进而导致心血管和脑血管疾病的发生。对于患有睡眠呼吸暂停的患者,这些情况可能会因间歇性缺氧而加剧。

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