由YAP介导的巨细胞极化与动脉样硬化的进展有关
Xin Zhang1, Xia Sun2, Qiaohong Qin1
1Institute of Basic and Translational Medicine, Xi'an Medical University, Xi'an, Shaanxi, 710021, China.
European journal of pharmacology
|November 7, 2025
概括
是的相关蛋白 (YAP) 通过通过CD36上调调节驱动M1巨细胞极化来促进动脉样硬化. 在巨细胞中抑制YAP为动脉样硬化提供了潜在的治疗策略.
科学领域:
- 心血管生物学 心血管生物学
- 免疫学 免疫学 免疫学
- 分子医学是分子医学.
背景情况:
- 大细胞两极分化是动脉样硬化发展的关键因素.
- 是的相关蛋白 (YAP) 影响巨细胞极化,但其在动脉样硬化中的特定作用尚未完全理解.
研究的目的:
- 为了研究YAP介导的巨细胞极化在动脉样硬化中的作用.
- 探索YAP作为动脉样硬化的潜在治疗点.
主要方法:
- 在使用高胆固醇饮食和AAV8-mPCSK9注射的小鼠中诱导动脉样硬化.
- 使用具有巨细胞特异性YAP删除 (YAPΔM) 的小鼠和ApoE-/-小鼠.
- 在巨细胞中以腺相关病毒 (AAV) 为媒介的针对YAP的shRNA的传递被用于治疗评估.
主要成果:
- 宏细胞特异性YAP删除减少了动脉样硬化斑块的大小,并促进了M2宏细胞的两极分化.
- YAP过度表达逆转了这些影响,表明YAP促进动脉样硬化.
- YAP通过TEAD4上调了CD36的表达,增强了氧化低密度脂蛋白 (ox-LDL) 的吸收和M1极化.
- 在ApoE-/-小鼠中,巨细胞特异性YAP敲除显著减轻了动脉样硬化.
结论:
- 通过通过TEAD4通过CD36上调调节诱导M1巨分极,YAP促进动脉样硬化.
- 在巨细胞中准YAP为动脉样硬化治疗提供了一个有希望的治疗途径.
关键词:
动脉样硬化是一种动脉样硬化.CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36 CD36巨细胞是一个巨细胞.是的 - 相关蛋白质.更多相关视频
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