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内皮细胞 (EC) 特定的Ctgf/Ccn2表达增加了EC重编程和动脉样硬化.

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关键词:
动脉硬化是因为动脉硬化.动脉样硬化斑块是一种动脉样硬化斑块.结合组织生长因子/CCN2内皮细胞是内皮细胞.纤维素-5 纤维素-5 是一种通过流量介导的动脉重塑.性差异的性别差异

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科学领域:

  • 血管生物学 血管生物学
  • 生物力学 生物力学
  • 细胞重编程 细胞重编程

背景情况:

  • 动脉内皮细胞 (ECs) 响应生物机械线索,如壁切应力和动脉硬.
  • 血流干扰和动脉硬度增加与炎症和纤维化有关,促进了病理性动脉重塑.
  • 连接流动干扰,度和EC重编程的现有途径仍然不完全理解.

研究的目的:

  • 研究ECs对结合硬化和流动干扰的反应的分子通路.
  • 为了确定关键的分子参与者和生物标志物参与EC重编程在这些病理条件下.
  • 测试这些途径的可变性,特别关注结缔组织生长因子 (CTGF).

主要方法:

  • 在纤维素-5淘汰赛 (Fbln5-/-) 的小鼠中使用了部分带绑定模型,以诱导硬化动脉中的流动干扰.
  • 进行生物力学测试以评估动脉硬性和量化斑块形成.
  • 产生的内皮细胞特异性Ctgf淘汰 (Ctgfecko) 小鼠,以调查CTGF的作用.
  • 在人类患者样本上使用免疫组织化学验证的结果 (心血管内关节切除术和外周动脉疾病).

主要成果:

  • 在流动受损的情况下,Fbln5-/-动脉模仿了患病的人类动脉的硬性,诱导了ECs的内皮转移到介质细胞转变 (EndMT).
  • 与野生型 (WT) 对照相比,硬的Fbln5-/-动脉中流动干扰导致动脉样斑块更容易受到伤害.
  • 结合组织生长因子 (CTGF) 在衰老,硬化和流动干扰条件下在EC上升调节,作为关键生物标志物.
  • 人类患者样本显示CTGF沉积增加在流动受损的区域.
  • 与WT对照组相比,雄性Ctgfecko小鼠在干扰的流动和动脉动脉的条件下表现出减少的斑块面积.
  • 雄性小鼠显示CTGF表达高于受扰流动的雌性小鼠.

结论:

  • 结合动脉硬化和流动干扰,引发了显著的EC重编程,并促进了病理性动脉重塑.
  • CTGF是这些生物力学驱动的血管变化的关键调解者和生物标志物.
  • 准CTGF可能提供治疗潜力,基于性别的差异影响其在动脉疾病进展中的作用.
  • 进一步研究纤维化通路的性别差异对于开发向疗法至关重要.