在小鼠中长期间歇性缺氧会诱导炎症途径,这与人类的睡眠呼吸暂停和脂肪肝炎有关
Jonathan Gaucher1, Emilie Montellier2, Guillaume Vial1
1Hypoxia and Physio-Pathology Laboratory (HP2) INSERM U1300, University Grenoble Alpes, INSERM U1300, and Grenoble Alpes University Hospital, Grenoble, France.
iScience
|February 2, 2024
概括
阻塞性睡眠呼吸暂停会导致间歇性缺氧,这是非酒精性脂肪肝疾病的关键驱动因素. 这项研究确定了分子链接和炎症生物标志物,建议对肝病患者进行睡眠呼吸暂停查.
科学领域:
- 肝病学 肝病学是一种肝病学.
- 睡眠医学 睡眠医学
- 免疫学 免疫学 免疫学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 通过间歇性缺氧 (IH) 与非酒精性脂肪性肝病 (NAFLD) 有关.
- 连接IH和NAFLD进展的分子机制,特别是免疫细胞的参与,仍然不太清楚.
研究的目的:
- 阐明IH,OSA和NAFLD病原体之间的分子联系.
- 为了确定与IH诱导的肝脏和全身炎症相关的生物标志物.
主要方法:
- 在长期暴露于IH的瘦小鼠中分析肝脏转录组学,脂组学和血清蛋白学.
- 与一组瘦骨OSA患者的转录组数据进行比较 (n=71).
主要成果:
- 长期的IH单独诱导了在人类数据中观察到的非酒精性脂肪肝炎 (NASH) 的分子特征.
- 确定了关键生物标志物,包括PPAR,NRF,酸,IL16,IL20,IFNB和TNF-α,与炎症有关.
结论:
- 建立了IH,OSA和脂肪肝炎之间的分子联系,突出了炎症作为中心途径.
- 建议确定分子特征作为NAFLD-OSA并发症的潜在诊断和治疗反应标志物.
- 倡导将OSA查纳入肝病表型化和探索治疗点.
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