Although both short and long sleep duration are associated with elevated hypertension risk, our understanding of their interplay with biological pathways governing blood pressure remains limited. To address this, we carried out genome-wide cross-population gene-by-short-sleep and long-sleep duration interaction analyses for three blood pressure traits (systolic, diastolic, and pulse pressure) in 811,405 individuals from diverse population groups. We discover 22 novel gene-sleep duration interaction loci for blood pressure, mapped to genes involved in neurological, thyroidal, bone metabolism, and hematopoietic pathways. Non-overlap between short sleep (12) and long sleep (10) interactions underscores the plausibility of distinct influences of both sleep duration extremes in cardiovascular health. With several of our loci reflecting specificity towards population background or sex, our discovery sheds light on the importance of embracing granularity when addressing heterogeneity entangled in gene-environment interactions, and in therapeutic design approaches for blood pressure management.

中文翻译：

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对来自不同人群的 811,405 名个体的血压基因-睡眠持续时间相互作用进行的大规模全基因组研究

尽管睡眠时间短和长都与高血压风险升高有关，但我们对它们与控制血压的生物途径相互作用的了解仍然有限。为了解决这个问题，我们对来自不同人群的 811,405 名个体的三种血压特征（收缩压、舒张压和脉压）进行了全基因组跨群体基因按短睡眠和长睡眠持续时间的相互作用分析。我们发现了 22 个新的血压基因与睡眠持续时间相互作用位点，映射到涉及神经、甲状腺、骨代谢和造血途径的基因。短睡眠 (12) 和长睡眠 (10) 相互作用之间的不重叠强调了两种极端睡眠时间对心血管健康的不同影响的合理性。由于我们的几个位点反映了人群背景或性别的特异性，我们的发现揭示了在解决基因-环境相互作用中的异质性以及血压管理的治疗设计方法时采用粒度的重要性。