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阻塞性睡眠呼吸暂停对心肌损伤和功能障碍的影响:一篇侧重于间歇性低氧分子机制的综述。

Effects of obstructive sleep apnea on myocardial injury and dysfunction: a review focused on the molecular mechanisms of intermittent hypoxia.

机构信息

Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 NanjingBei Street, Heping District, Shenyang, 110001, Liaoning Province, China.

Clinical Medical Research Center of Imaging in Liaoning Province, The First Hospital of China Medical University, No. 155 NanjingBei Street, Heping District, Shenyang, 110001, Liaoning Province, China.

出版信息

Sleep Breath. 2024 Mar;28(1):41-51. doi: 10.1007/s11325-023-02893-2. Epub 2023 Aug 7.

DOI:10.1007/s11325-023-02893-2
PMID:37548920
Abstract

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and is strongly associated with adverse cardiovascular outcomes. Myocardial injury and dysfunction have been commonly observed in clinical practice, particularly in patients with severe OSA. However, the underlying mechanisms remain obscure. In this review, we summarized the molecular mechanisms by which IH impact on myocardial injury and dysfunction. In brief, IH-induced cardiomyocyte death proceeds through the regulation of multiple biological processes, including differentially expressed transcription factors, alternative epigenetic programs, and altered post-translational modification. Besides cell death, various cardiomyocyte injuries, such as endoplasmic reticulum stress, occurs with IH. In addition to the direct effects on cardiomyocytes, IH has been found to deteriorate myocardial blood and energy supply by affecting the microvascular structure and disrupting glucose and lipid metabolism. For better diagnosis and treatment of OSA, further studies on the molecular mechanisms of IH-induced myocardial injury and dysfunction are essential.

摘要

阻塞性睡眠呼吸暂停(OSA)的特征是间歇性低氧(IH),并与不良心血管结局密切相关。心肌损伤和功能障碍在临床实践中很常见,特别是在严重 OSA 患者中。然而,其潜在机制尚不清楚。在这篇综述中,我们总结了 IH 影响心肌损伤和功能障碍的分子机制。简而言之,IH 诱导的心肌细胞死亡通过调节多种生物过程来进行,包括差异表达的转录因子、替代表观遗传程序和改变的翻译后修饰。除了细胞死亡,各种心肌损伤,如内质网应激,也会随着 IH 而发生。除了对心肌细胞的直接影响外,IH 通过影响微血管结构和破坏葡萄糖和脂质代谢,还会恶化心肌的血液和能量供应。为了更好地诊断和治疗 OSA,有必要进一步研究 IH 诱导的心肌损伤和功能障碍的分子机制。

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