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通过miR-141-3p/PDCD4轴,COPD呼吸道上皮细胞衍生的细胞外囊泡通过miR-141-3p/PDCD4轴促进内皮功能障碍和动脉样硬化

Zihan Wang¹, Jun Shi¹, Ying Liang¹

¹Department of Respiratory and Critical Care Medicine, Research Center for Chronic Airway Diseases, Peking University Third Hospital; Peking University Health Science Center, Beijing, China.

Journal of nanobiotechnology

|February 7, 2026

概括

来自慢性阻塞性肺病 (COPD) 气道细胞的细胞外囊泡通过降低miR-141-3p的调节促进动脉样硬化. 恢复miR-141-3p可能治疗COPD相关的心血管并发症.

科学领域:

肺部医学肺部医学
心血管研究研究心血管研究
分子生物学分子生物学

背景情况:

慢性阻塞性肺病 (COPD) 经常与心血管疾病 (CVD) 共存,但根本机制尚不清楚.
细胞外囊泡 (EVs) 调解细胞通信,并可能将COPD与动脉样硬化联系起来.
这项研究调查了COPD呼吸道上皮细胞 (AEC) 的EV是否会导致内皮功能障碍和动脉样硬化.

研究的目的:

确定COPD AEC衍生的EVs在内皮功能障碍和动脉样硬化中的作用.
阐明COPDEVs影响血管健康的分子机制,包括microRNA参与.
探索针对EV中的特定微RNA治疗COPD相关心血管疾病的治疗潜力.

主要方法:

从COPD患者和对照AEC中分离的EVs.
在体外对内皮细胞 (炎症,细胞亡,单细胞粘附) 评估了EV的影响.
向ApoE-/-小鼠注射EV以评估动脉样硬化斑块的发展;确定了microRNA并验证了miR-141-3p/PDCD4相互作用;测试了miR-141-3p补充剂.

主要成果:

慢性肺炎AEC-EV增加了内皮炎症,细胞亡和单细胞粘附.
在老鼠中,COPD衍生的EV加速了动脉样硬化.
在COPD下调 miR-141-3p EVs 向PDCD4,破坏PDCD4/NF-κB信号传递;miR-141-3p恢复减少了血管损伤和动脉样硬化.

结论:

通过miR-141-3p下调,PDCD4失调和NF-κB激活,COPD AEC衍生的EVs促进动脉样硬化心血管疾病.
这一途径代表了一种将COPD与心血管并发症联系起来的新机制.
miR-141-3p被确定为缓解COPD患者血管问题的潜在治疗标.

关键词:

动脉样硬化是一种动脉样硬化.心血管疾病是什么心血管疾病慢性阻塞性肺病是一种慢性阻塞性肺病.伴随性疾病伴随性疾病细胞外囊泡中的细胞外囊泡.

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