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首页> 外文期刊>BMC Medical Genomics >Polymorphisms in nitric oxide synthase and endothelin genes among children with obstructive sleep apnea
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Polymorphisms in nitric oxide synthase and endothelin genes among children with obstructive sleep apnea

机译：阻塞性睡眠呼吸暂停患儿一氧化氮合酶和内皮素基因多态性

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Background Obstructive sleep apnea (OSA) is associated with adverse and interdependent cognitive and cardiovascular consequences. Increasing evidence suggests that nitric oxide synthase ( NOS ) and endothelin family ( EDN ) genes underlie mechanistic aspects of OSA-associated morbidities. We aimed to identify single nucleotide polymorphisms (SNPs) in the NOS family (3 isoforms), and EDN family (3 isoforms) to identify potential associations of these SNPs in children with OSA. Methods A pediatric community cohort (ages 5–10 years) enriched for snoring underwent overnight polysomnographic (NPSG) and a fasting morning blood draw. The diagnostic criteria for OSA were an obstructive apnea-hypopnea Index (AHI) >2/h total sleep time (TST), snoring during the night, and a nadir oxyhemoglobin saturation Results For NOSA vs. OSA groups, 15 differentially distributed SNPs for NOS1 gene, and 1 SNP for NOS3 emerged, while 4 SNPs for EDN1 and 1 SNP for both EDN2 and EDN3 were identified. However, in the smaller sub-group for whom endothelial function was available, none of the significant SNPs was retained due to lack of statistical power. Conclusions Differences in the distribution of polymorphisms among NOS and EDN gene families suggest that these SNPs could play a contributory role in the pathophysiology and risk of OSA-induced cardiovascular morbidity. Thus, analysis of genotype-phenotype interactions in children with OSA may assist in the formulation of categorical risk estimates.
机译：背景阻塞性睡眠呼吸暂停（OSA）与不良和相互依存的认知和心血管后果相关。越来越多的证据表明，一氧化氮合酶（NOS）和内皮素家族（EDN）基因是与OSA相关的发病机制的基础。我们旨在鉴定NOS家族（3个亚型）和EDN家族（3个亚型）中的单核苷酸多态性（SNP），以识别OSA儿童中这些SNP的潜在关联。方法对一小儿（5〜10岁）社区进行打呼enrich训练，并对其进行夜间通宵多导睡眠监测（NPSG）和空腹早晨抽血。 OSA的诊断标准是阻塞性呼吸暂停低通气指数（AHI）> 2 / h总睡眠时间（TST），夜间打呼，和最低氧合血红蛋白饱和度结果NOSA与OSA组相比，NOS1的15种差异分布的SNP基因，出现NOS3的1个SNP，而鉴定出EDN1的4个SNP和EDN2和EDN3的1个SNP。但是，在具有内皮功能的较小亚组中，由于缺乏统计能力，没有保留任何重要的SNP。结论NOS和EDN基因家族之间的多态性分布差异表明，这些SNP可能在OSA诱发的心血管疾病的病理生理和风险中起重要作用。因此，对OSA儿童的基因型-表型相互作用的分析可能有助于制定分类风险评估。

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