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白三烯作为阻塞性睡眠呼吸暂停与动脉粥样硬化之间的分子联系。

Leukotrienes as a molecular link between obstructive sleep apnoea and atherosclerosis.

机构信息

Université Grenoble Alpes, Grenoble F-38041, France.

出版信息

Cardiovasc Res. 2014 Feb 1;101(2):187-93. doi: 10.1093/cvr/cvt247. Epub 2013 Nov 7.

Abstract

Leukotrienes are biologically active lipid mediators of inflammation involved in atherogenesis. Obstructive sleep apnoea (OSA) patients exhibit early atherosclerosis and activation of the leukotriene pathway. In OSA patients, the production of leukotrienes is increased in relation to OSA severity and in vitro exposure of immune cells to intermittent hypoxia increases leukotriene pathway transcription. Moreover, the leukotriene transcriptional pathway is associated with early vascular remodelling. Lastly, obesity is a major confounding factor for leukotriene activation in OSA. The aim of this review was to focus on the intricate network of leukotrienes, chronic intermittent hypoxia, and atherosclerosis, with an emphasis on the role of leukotrienes in the early atherosclerosis observed in OSA patients.

摘要

白三烯是参与动脉粥样硬化形成的具有生物活性的炎症脂质介质。阻塞性睡眠呼吸暂停(OSA)患者表现出早期动脉粥样硬化和白三烯途径的激活。在 OSA 患者中,白三烯的产生与 OSA 严重程度有关,体外免疫细胞暴露于间歇性低氧会增加白三烯途径的转录。此外,白三烯转录途径与早期血管重塑有关。最后,肥胖是 OSA 中白三烯激活的一个主要混杂因素。本综述的目的是重点关注白三烯、慢性间歇性低氧和动脉粥样硬化之间复杂的网络关系,强调白三烯在 OSA 患者中观察到的早期动脉粥样硬化中的作用。

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