Obstructive sleep apnea syndrome (OSAHS) is a widespread respiratory dysfunction that has attracted more and more attention in recent years. Recently, a large number of studies have shown that abnormal DNA methylation epigenetically silences genes necessary for the pathogenesis of human diseases. However, the exact mechanism of abnormal DNA methylation in OSAHS is still elusive. In this study, we downloaded the OSAHS data from the GEO database. Our data for the first time revealed 520 hypermethylated genes and 889 hypomethylated genes in OSAHS. Bioinformatics analysis revealed that these abnormal methylated genes exhibited an association with the regulation of angiogenesis, apoptosis, Wnt, and ERBB2 signaling pathways. PPI network analysis displayed the interactions among these genes and validated several hub genes, such as GPSM2, CCR8, TAS2R20, TAS2R4, and TAS2R5, which were related to regulating liganded Gi-activating GPCR and the transition of mitotic metaphase/anaphase. In conclusion, our study offers a new hint of understanding the molecular mechanisms in OSAHS progression and will provide OSAHS with newly generated innovative biomarkers.

中文翻译：

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确定阻塞性睡眠呼吸暂停低通气综合征的甲基化DNA驱动的关键基因。

阻塞性睡眠呼吸暂停综合症（OSAHS）是一种广泛的呼吸功能障碍，近年来已引起越来越多的关注。最近，大量研究表明，异常的DNA甲基化从表观遗传学上沉默了人类疾病发病机理所必需的基因。但是，OSAHS中异常的DNA甲基化的确切机制仍然难以捉摸。在这项研究中，我们从GEO数据库下载了OSAHS数据。我们的数据首次揭示了OSAHS中的520个高甲基化基因和889个低甲基化基因。生物信息学分析表明，这些异常的甲基化基因与血管生成，凋亡，Wnt和ERBB2信号通路的调节有关。PPI网络分析显示了这些基因之间的相互作用，并验证了多个集线器基因，例如GPSM2，CCR8，TAS2R20，TAS2R4和TAS2R5与调节配体的Gi激活GPCR和有丝分裂中期/后期的过渡有关。总之，我们的研究为理解OSAHS进展中的分子机制提供了新的提示，并将为OSAHS提供新产生的创新生物标志物。