通过动脉内皮细胞的LDL转细胞化 - 动脉样硬化通过一千个切口?
Tse Wing Winnie Ho1,2, Andria Henry2,3, Warren L Lee4,5,6,7,8
1Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
Current atherosclerosis reports
|June 26, 2023
概括
低密度脂蛋白 (LDL) 通过内皮细胞的转细胞形成,有助于动脉样硬化. 新的研究揭示了像SR-BI和ALK1这样的关键分子参与者,为管理这一过程提供了潜在的治疗点.
科学领域:
- 心血管生物学 心血管生物学
- 内皮细胞生物学 内皮细胞生物学
- 动脉样硬化研究 动脉样硬化研究
背景情况:
- 低密度脂蛋白 (LDL) 在动脉内脏中的积累是动脉样硬化发展的关键早期阶段.
- 现在已经认识到,通过内皮单层的LDL的转细胞化对内密沉积有重大贡献.
研究的目的:
- 审查最近关于LDL转细胞化的发现.
- 探索治疗性操纵LDL转细胞的潜力.
主要方法:
- 使用全内反射光显微镜 (TIRF) 进行活细胞成像.
- 研究参与LDL转细胞化的分子媒介.
主要成果:
- LDL 转细胞因子的介导是由清除器受体类B型1 (SR-BI) 和活性因子受体类激酶1 (ALK1) 的介导.
- 雌激素通过降低SR-BI的调节来抑制LDL转细胞形成.
- 高流动性组盒子1 (HMGB1) 蛋白质促进LDL转细胞.
- 通过ALK1介导的细胞转移独立于其激酶活性,并且受到BMP9.9的反对.
- 炎症过程刺激了LDL转细胞.
结论:
- 了解LDL转细胞的机制对于开发新的动脉样硬化疗法至关重要.
- 针对SR-BI,ALK1,HMGB1或它们的相互作用等介质是一个潜在的治疗策略.
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