氨酸在过敏性喘中增加,并促进呼吸道重塑
Tingting Xu1, Zhenzhen Wu1, Qi Yuan1
1Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
JCI insight
|July 11, 2023
概括
氨酸及其酶PYCR1在喘中升高,导致呼吸道重塑和EMT. 准PYCR1或普林可能提供新的喘治疗方法.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- oline和pyrroline-5-carboxylate降解酶1 (PYCR1) 与上皮细胞-介质细胞过渡 (EMT) 有关.
- 林和PYCR1在通过EMT进行过敏喘气道改造中的作用尚不清楚.
研究的目的:
- 调查林和PYCR1在过敏性喘气道改造中的参与.
- 探索针对林和PYCR1治疗喘的治疗潜力.
主要方法:
- 在喘患者和室内灰尘虫 (HDM) 诱导的小鼠模型中评估了proline和PYCR1水平.
- 使用PYCR1淘汰赛小鼠和治疗性PYCR1抑制.
- 检查了EMT,线粒体分裂,代谢重编程和信号通路 (AKT/mTORC1,WNT3a/β-catenin).
主要成果:
- 在喘患者和暴露于HDM的小鼠中,血中proline和PYCR1的升高.
- 在小鼠中,PYCR1缺乏减少了普罗林水平,呼吸道重塑和EMT.
- 失去PYCR1通过调节线粒体和信号通路来抑制HDM诱导的EMT.
- 抑制PYCR1和林剥夺部分缓解了呼吸道重塑.
结论:
- 林和PYCR1在通过EMT对过敏性喘呼吸道重塑中发挥着重要作用.
- PYCR1和普罗林代表了喘管理的潜在治疗点.
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