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素饮食驱动肠道炎症和外体 miR-17-3p 升高在异常性矮身症患者中

Yameng Wang^1,2,3,4, Zhiwen Wu^1,2,3,4, Jinghong Yuan^1,2,3,4

¹Department of Orthopedics, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang City, Jiangxi Province, China.

Nature communications

|December 30, 2025

概括

儿童的异常矮身 (ISS) 与外体内miR-17-3p的升高有关,可能是由辛饮食引发的. 这种分子会破坏生长,但有针对性的疗法显示出有前途.

科学领域:

儿科内分泌学儿科内分泌学
分子生物学分子生物学
异构体生物学异构体生物学

背景情况:

异形性矮身 (ISS) presents一个重要的儿科挑战,未知病因和可变的生长激素 (GH) 治疗反应.
患有ISS的儿童的等离子体外基因组显示人体序列A-microRNA-17-3p (hsa-miR-17-3p) 的水平增加.
这种微RNA破坏了关键的生长信号通路,并损害了软骨细胞的增殖.

研究的目的:

为了研究外体hsa-miR-17-3p在ISS病变发生中的作用.
探索潜在的环境触发因素,如饮食因素,有助于国际空间站.
为国际空间站开发和测试新的治疗策略.

主要方法:

在患有ISS的儿童中分析血外体含量 (hsa-miR-17-3p).
开发一种富含素的食,模仿国际空间站的老鼠模型.
在老鼠和国际空间站儿童中评估肠道炎症和外体 miRNA 概况.
在体内测试工程外体以沉默hsa-miR-17-3p结合GH治疗.

主要成果:

在ISS儿童的血外体中增加的hsa-miR-17-3p抑制了ZNF148/SOS1信号传递.
在大鼠中,富含素的饮食诱导了类似ISS的表型,具有增加的血hsa-miR-17-3p和肠道炎症.
国际空间站儿童的便样本显示hsa-miR-17-3p和炎症标志物升高,这表明与辛饮食有关.
使用工程外体和GH的联合治疗恢复了生长板功能.

结论:

一个涉及hsa-miR-17-3p的饮食驱动的外体轴为ISS做出了贡献.
饮食因素,特别是素,可能会引发肠道炎症和随后的外生体变化导致ISS.
基于外体的向治疗为管理ISS提供了一个有希望的新策略,特别是在素消费量高的地区.

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