过度伸展会导致血管光滑肌肉细胞中的脂质积累,这些细胞依赖NADPH氧化酶1的作用
Jiazhen Zhang1, Qinfen Li1, Suoqi Ding2
1College of Life Sciences, University of Chinese Academy of Sciences, Beijing 101408, China.
Mechanobiology in medicine
|May 21, 2025
概括
脉动动脉拉伸促进血管光滑肌细胞 (VSMC) 脂质积累和泡细胞的形成,通过上调NOX1. 抑制NOX1或活性氧物种 (ROS) 阻止了这一过程,揭示了动脉样硬化的新机制.
科学领域:
- 心血管生物学 心血管生物学
- 细胞机械传导 细胞机械传导
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 动脉样硬化症的特征是含脂的泡细胞,通常来自血管光滑肌细胞 (VSMC).
- 在动脉流条件下,驱动VSMC转化为泡细胞的精确机制仍然不完全理解.
研究的目的:
- 阐明机械拉伸在VSMC泡细胞形成中的作用.
- 研究NADPH氧化酶1 (NOX1) 和活性氧物种 (ROS) 在这个过程中的参与.
主要方法:
- 一个微流体装置被用来在24小时内向VSMC应用循环拉伸 (15%,0.05Hz).
- 评估了NOX1和CD36的蛋白质表达.
- 细胞内脂质积累的量化.
- 评估了NOX1抑制,ROS清除和NOX1敲击的效果.
- 我们检查了JAK/STAT信号通路.
主要成果:
- 循环拉伸显著增加了VSMCs的细胞内脂质积累.
- 伸展也导致NOX1和CD36.6的蛋白质表达增加.
- 抑制NOX1活性,ROS清除或NOX1倒置显著降低了脂质积累.
- 在拉伸过程中NOX1上调与JAK/STAT信号通路有关.
结论:
- 机械拉伸通过NOX1依赖的ROS生产诱导VSMC泡细胞的形成.
- 在JAK/STAT路径中介NOX1上调调节以应对伸展.
- 这项研究揭示了一种新的机制,有助于动脉样硬化发展.
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