阻塞性睡眠呼吸暂停（OSA）的特征是间歇性缺氧（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常见，尤其是重度OSA患者。然而,潜在的机制仍然模糊。在这次审查中,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个生物学过程进行，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,各种心肌细胞损伤，如内质网应激，发生在IH。除了对心肌细胞的直接影响，已发现IH通过影响微血管结构并破坏葡萄糖和脂质代谢而使心肌血液和能量供应恶化。为了更好地诊断和治疗OSA，进一步研究IH诱导的心肌损伤和功能障碍的分子机制至关重要。
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.
