通过对转录基因和蛋白质基因的综合性分析,确定了一种涉及慢性阻断性睡眠呼吸暂停与心房动相关的新目标
Jun Shen1,2, Junqing Liang1,2, Manzeremu Rejiepu1,2
1Xinjiang Key Laboratory of Cardiac Electrophysiology and Cardiac Remodeling, The First Affiliated Hospital of Xinjiang Medical University, Urumqi, Xinjiang, People's Republic of China.
Journal of inflammation research
|December 5, 2023
概括
慢性阻塞性睡眠呼吸暂停 (COSA) 通过激活GSTZ1,从而损害线粒体,增加了心房动 (AF) 的风险. 切除状交会降低这种效果,这表明GSTZ1是COSA相关的AF的治疗标.
科学领域:
- 心脏病学 心脏病学
- 睡眠医学 睡眠医学
- 分子生物学分子生物学
背景情况:
- 心房动 (AF) 是一种与慢性阻塞性睡眠呼吸暂停 (COSA) 相关的严重并发症.
- 将COSA与AF联系在一起的分子机制仍然不完全理解.
- 识别新的分子点对于开发有效的治疗方法至关重要.
研究的目的:
- 为了识别与COSA相关的AF中涉及的分子点.
- 调查转录组和蛋白质组改变在COSA诱导的AF中的作用.
- 探讨状缩切除术在缓解COSA相关的AF方面的潜力.
主要方法:
- 在12周的时间里,在小猎犬中建立了一个COSA模型.
- 组包括对照组,OSA和OSA与左上腺移除 (OSA+GP).
- 在心房样本上进行了电生理学研究,组织学,转录组学和蛋白质组学.
主要成果:
- 与对照组相比,OSA显著增加了AF诱导性和AF持续时间.
- 综合分析揭示了许多基因和蛋白质在不同群体之间表达的差异.
- 线粒体功能障碍是受影响的关键途径,GSTZ1被确定为OSA中的关键激活分子,由GP消去逆转.
结论:
- 在COSA中,GSTZ1激活似乎是线粒体损伤和AF基质形成的核心.
- 状移除可以通过调节GSTZ1.1来抵消COSA诱导的AF.
- 在COSA患者中,GSTZ1代表了管理AF的潜在治疗标.
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