S100a8和s100a9在中度至重度阻塞性睡眠呼吸暂停综合征患者的大动脉壁中升高
Ewa Migacz1, Wioletta Olejarz2,3, Andrzej Łoś4
1Department of Otorhinolaryngology, Faculty of Medicine and Dentistry, Medical University of Warsaw, Warsaw, Poland.
Sleep & breathing = Schlaf & Atmung
|July 8, 2025
概括
中度至重度的阻塞性睡眠呼吸暂停 (OSA) 与大动脉组织中炎症前驱S100A8和S100A9蛋白质的增加有关. 这些发现表明在OSA相关的血管炎症和动脉样硬化中发挥了作用.
科学领域:
- 心血管研究研究心血管研究
- 睡眠医学 睡眠医学
- 炎症生物学 炎症生物学
背景情况:
- 阻塞性睡眠呼吸暂停 (OSA) 与全身炎症和诸如动脉样硬化等心血管疾病有关.
- S100A8和S100A9是参与动脉动脉生成的促炎蛋白.
- 在OSA患者中S100A8/S100A9的大动脉表达以前是未知的.
研究的目的:
- 为了研究OSA严重程度和大动脉组织中S100A8 / S100A9表达之间的关系.
- 在接受冠状动脉旁路移植 (CABG) 的患者中评估大动脉S100A8/S100A9水平.
主要方法:
- 根据家庭睡眠呼吸暂停测试 (WatchPATTM),接受CABG的46名患者被分为控制,轻度OSA和中度至重度OSA组.
- 在手术期间获得了大动脉壁样本.
- 免疫组织化学被用来测量S100A8和S100A9的表达.
- 统计分析比较了OSA严重程度组中的蛋白质水平.
主要成果:
- 中度至重度的OSA患者在主动脉组织中显示出显著更高的S100A9表达 (p<0.01).
- 在中度至重度OSA患者中观察到S100A8表达的非显著增加趋势 (p=0.073).
- 这两种蛋白质都在患有更严重的OSA的患者的大动脉中升高,与对照组和轻度OSA相比.
结论:
- S100A8和S100A9在中度至重度OSA患者的大动脉壁中过度表达.
- 这些蛋白质可能会导致与OSA相关的血管炎症和动脉样硬化.
- 需要进一步的研究来探索S100A8 / S100A9作为潜在的生物标志物或OSA相关心血管疾病的治疗点.
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