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微血管内皮细胞许可 APS血管病通过YAP1和CCN2介导的信号

Hui Shi^1,2, Wenying Liang², Zhixia Yang¹

¹Department of Rheumatology and Immunology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China (H.S., Z.Y., Z.D., H.P., C.Y.).

|August 29, 2025

概括

抗脂综合征 (APS) 血管病包括异常的细胞增殖. 这项研究确定了CCN2作为关键调解剂,并建议使用抗CCN2抗体作为APS的潜在治疗策略.

科学领域:

血管生物学
免疫学
细胞信号传输

背景情况:

抗脂综合征 (APS) 与大血管血栓形成有关.
由于内皮细胞和光滑肌肉细胞的增殖,APS血管病包括微血管封闭.
目前缺乏针对APS血管病的机制和向治疗方法.

研究的目的:

研究APS血管病变的细胞和分子机制.
确定参与APS微血管内皮细胞 (MVEC) 功能障碍的关键调解者.
探索潜在的治疗点.

主要方法:

APS患者皮肤活检的单细胞RNA测序.
免疫光显微镜和ELISA检测CCN1和CCN2.
在体外培养MVEC与APS患者的IgG以分析信号通路 (TLR4,YAP1).
评估血管光滑肌细胞的增殖和迁移.
在体外和APS小鼠模型中对抗CCN2单克隆抗体的评估.

主要成果:

在APS内皮细胞和血中增加CCN1和CCN2表达.
通过TLR4和YAP1信号传递,诱导了APS患者的IgGCCN1和CCN2上调.
通过抗CCN2抗体抑制,促进了血管光滑肌细胞的增殖和迁移.
在APS脏活检中观察到CCN2和YAP1核转位的增加.
在APS小鼠模型中,抗CCN2抗体治疗降低了新内的形成.

结论:

在APS皮肤微血管中激活YAP1介导的信号.
在APS中,CCN2是YAP1的点,它介导着MVEC和血管光滑肌细胞之间的增殖信号传递.
针对CCN2提供了一个潜在的治疗策略.

关键词:

其他国家一个 YAP 抗脂综合征内皮细胞微血管 APS 新心的形成血管平滑肌细胞

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