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内皮BMP6驱动血液动力学依赖的VSMCs在动脉样硬化中的化

Shen Li^1,2,3, Shuang Cao^1,2,3,4,5, Peipei Li^2,6

¹The Department of Neurology, the First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, 12636, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|October 13, 2025

概括

骨形态遗传蛋白6 (BMP6) 在动脉样硬化 (CAS) 中驱动血管化. 这一过程涉及内皮细胞与血管平滑肌肉细胞的相互作用,并受到血液动力学压力的影响,突出显示了BMP6作为治疗点.

科学领域:

心血管生物学心血管生物学
动脉样硬化的分子机制
血管化血管化

背景情况:

动脉样硬化 (CAS) 是缺血性中风的重要原因,血管化加剧了疾病的进展.
在CAS中控制血管化的精确分子路径尚未完全理解.
骨形态遗传蛋白 (BMPs) 与化有关,但BMP6信号的作用尚不清楚.

研究的目的:

为了研究BMP6在动脉动脉样硬化中的血管化中的作用.
阐明BMP6与CAS中的化联系的潜在分子机制.

主要方法:

人类CAS斑块的单细胞RNA测序,以识别细胞-细胞相互作用和基因表达模式.
使用内皮细胞 (EC) 和血管光滑肌细胞 (VSMC) 进行体外研究,以评估BMP6功能.
在体内实验中使用内皮特异性的BMP6淘汰 (BMP6^ECKOApoE^-/-) 和过度表达的小鼠模型.
对血流干扰对BMP6表达和化的影响进行分析.

主要成果:

单细胞RNA测序揭示了具有高BMP6表达的EC通过BMP信号与VSMC相互作用.
在体外,BMP6直接诱导了VSMC的骨质分化.
BMP6激活了SMAD的信号通路.
特定于内皮细胞的BMP6淘汰会减少性损伤,而过度表达会加剧这些损伤.
干扰的流量条件通过抑制克鲁佩尔样因子4增加了BMP6的表达,将血动力学力与化联系起来.

结论:

BMP6是心动脉动脉样硬化中血管化的关键调节者.
由BMP6介导的EC-VSMC通信,受血动力应激的影响,驱动化.
准BMP6信号传输为CAS提供了一个潜在的治疗策略.

关键词:

动脉动脉样硬化 - 动脉动脉样硬化细胞交叉通话细胞交叉通话血液动力学血液动力学一个单细胞RNA测序.血管化血管化

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