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大 EHD1 促进炎症,稳定索尔提林,加速动脉样硬化

Fanglin Ma, Yu Liu, Yang Xu

bioRxiv : the preprint server for biology

|November 24, 2025

概括

内细胞调节器EHD1通过通过TNFR2-NF-kB信号传递和稳定sortilin来增强巨细胞炎症来促进动脉样硬化. 删除EHD1可以减少病变大小和动脉样硬化中的炎症反应.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
心血管研究的心血管研究.

背景情况:

巨细胞对于动脉样硬化发展至关重要,通过细胞表面受体调节免疫反应.
炎症刺激和内细胞贩运对巨细胞受体调节的理解尚不完全.
细胞内膜流通对于维持细胞表面受体平衡至关重要.

研究的目的:

研究内细胞调节器EHD1在巨细胞免疫反应中的作用.
确定EHD1对动脉样硬化进展的贡献.

主要方法:

在小鼠和人类动脉样硬化斑块中使用scRNA-seq和免疫光检测评估了EHD1的表达.
在Ldlr-/-小鼠中利用骨髓移植 (BMT) 来评估EHD1删除对动脉样硬化的影响.
在骨髓衍生的巨细胞上进行了体外机械学研究,包括炎症和内细胞化试验.

主要成果:

在老鼠和人类中,随着动脉样硬化的进展,EHD1的表达增加.
在BMT小鼠中删除EHD1减少了动脉样硬化病变的大小和减弱的炎症反应.
EHD1加速TNFR2内细胞循环,激活NF-kB信号传递并增加炎症性细胞因子.
EHD1与复原体相互作用,稳定索尔提林,这是已知的动脉样硬化风险因素.

结论:

EHD1通过通过TNFR2-NF-kB信号传递和sortilin稳定增强巨细胞炎症来促进动脉样硬化.
这项研究确定了EHD1介导的膜贩运在巨细胞功能中的新角色.
研究结果表明,潜在的治疗策略是针对动脉样硬化中失调的膜贩运.

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