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CCAT1通过STAU1-介导的IRF1mRNA降解减轻间歇性缺氧相关的内皮细胞灭

Wen Liu¹, Xinxin Li¹, Qing Zhu¹

¹Department of Cardiovascular Ultrasound, The First Hospital of China Medical University, No. 155 NanjingBei Street, Heping District, Shenyang, Liaoning Province, 110001, China; Clinical Medical Research Center of Imaging in Liaoning Province, The First Hospital of China Medical University, No. 155 NanjingBei Street, Heping District, Shenyang, Liaoning Province, 110001, China.

Biochimica et biophysica acta. Molecular basis of disease

|January 11, 2026

概括

长非编码RNACCAT1通过降低热致死来保护阻塞性睡眠呼吸暂停 (OSA) 中的内皮功能障碍. 这一发现为与OSA相关的血管问题提供了潜在的治疗策略.

科学领域:

分子生物学分子生物学
心血管研究研究心血管研究
睡眠医学睡眠医学

背景情况:

血管内皮功能障碍在阻塞性睡眠呼吸暂停 (OSA) 患者中很常见.
连接间歇性缺氧 (IH) 与内皮功能障碍的确切机制尚未完全理解.

研究的目的:

研究 lncRNA CCAT1 和 GSDMD 在IH引起的内皮功能障碍中的作用.
在OSA的背景下阐明CCAT1/IRF1/GSDMD路径.

主要方法:

生物信息分析用于识别IH中的关键分子.
在OSA患者中,血清CCAT1和GSDMD水平与内皮功能之间的相关性分析.
使用IH诱导的人类静脉内皮细胞 (HUVEC) 进行体外研究,以评估CCAT1,IRF1和热.

主要成果:

生物信息学确定了 pyroptosis 是IH的一个关键途径.
OSA患者的血清GSDMD增加和CCAT1降低,与OSA严重程度和内皮功能障碍相关.
在IH诱导的HUVEC中,CCAT1被下调,IRF1被上调,CCAT1过度表达通过降解IRF1mRNA降低了热和改善了内皮功能.

结论:

lncRNA CCAT1通过STAU1-介导的IRF1mRNA降解来减弱IH诱导的内皮质质炎.
CCAT1证明了作为OSA相关的内皮功能障碍的治疗标的潜力.

关键词:

在CCAT1中使用.间歇性缺氧间歇性缺氧热灭菌的发生.在STAU1中介的mRNA降解过程中.

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