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<p>Idiopathic short stature (ISS) remains a major pediatric challenge with unclear causes and inconsistent responses to growth hormone therapy. Here we show that plasma exosomes from children with ISS contain elevated <i>hsa-miR-17-3p</i> that disrupts growth signaling and impairs cartilage cell proliferation. Elevated <i>miR-17-3p</i> suppresses ZNF148/SOS1 signaling, linking molecular dysfunction to dietary exposure in ISS. To investigate environmental triggers, we developed a capsaicin-rich diet rat model that recapitulates ISS, showing normal Gh/Igf-1 levels but elevated plasma <i>miR-17-3p</i>. The diet induced mild gut inflammation, increasing <i>miR-17-3p</i> in intestinal and plasma exosomes. Fecal samples from ISS children exhibited similar elevations in <i>miR-17-3p</i> and inflammatory markers, linking spicy diets to ISS pathogenesis. Finally, engineered exosomes designed to silence <i>miR-17-3p</i>, combined with localized growth hormone therapy, restored growth plate function. These findings uncover a diet-driven exosome axis underlying ISS and suggest new therapeutic strategies for children in high-capsaicin regions.</p>

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Capsaicin diet drives gut inflammation and exosomal miR-17-3p elevation in idiopathic short stature

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月30日

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  • Yameng Wang,
  • Zhiwen Wu,
  • Jinghong Yuan,
  • Junchao Zhu,
  • Marco Ventin,
  • Shahrzad Arya,
  • Peng Yu,
  • Giulia Cattaneo,
  • Guowen Huang,
  • Wenrui Zhao,
  • Shengqin Li,
  • Junqiu Zhang,
  • Qi Chen,
  • Xinhui Wang,
  • Lianyong Li,
  • Xijuan Liu,
  • Xigao Cheng,
  • Jingyu Jia

摘要

Idiopathic short stature (ISS) remains a major pediatric challenge with unclear causes and inconsistent responses to growth hormone therapy. Here we show that plasma exosomes from children with ISS contain elevated hsa-miR-17-3p that disrupts growth signaling and impairs cartilage cell proliferation. Elevated miR-17-3p suppresses ZNF148/SOS1 signaling, linking molecular dysfunction to dietary exposure in ISS. To investigate environmental triggers, we developed a capsaicin-rich diet rat model that recapitulates ISS, showing normal Gh/Igf-1 levels but elevated plasma miR-17-3p. The diet induced mild gut inflammation, increasing miR-17-3p in intestinal and plasma exosomes. Fecal samples from ISS children exhibited similar elevations in miR-17-3p and inflammatory markers, linking spicy diets to ISS pathogenesis. Finally, engineered exosomes designed to silence miR-17-3p, combined with localized growth hormone therapy, restored growth plate function. These findings uncover a diet-driven exosome axis underlying ISS and suggest new therapeutic strategies for children in high-capsaicin regions.