肥胖脂肪细胞通过TGF-β1信号传递诱导纤维细胞向肌纤维细胞的转变:喘病原发生的影响
Nour Jalaleddine1, Mahmood Hachim1, Alexander Giddey2
1College of Medicine, Mohammed Bin Rashid University of Medicine and Health Sciences, Dubai Health, Dubai, United Arab Emirates.
American journal of physiology. Lung cellular and molecular physiology
|February 21, 2026
概括
肥胖通过促进气道纤维化使喘恶化. 肥胖脂肪细胞通过转化生长因子-β (TGF-β) 途径刺激纤维细胞到肌纤维细胞的过渡 (FMT),特别是在喘患者中.
科学领域:
- 肺部医学 肺部医学
- 细胞生物学 细胞生物学
- 免疫学 免疫学 免疫学
背景情况:
- 肥胖是严重喘的重要危险因素,导致治疗结果较差.
- 脂肪细胞 (脂肪细胞) 在气道壁中被发现,它们的存在与人体质量指数 (BMI) 相相关.
- 呼吸道脂肪细胞在喘病变,特别是呼吸道纤维化中的特定作用尚不清楚.
研究的目的:
- 研究脂肪细胞在通过纤维细胞到肌纤维细胞过渡 (FMT) 促进呼吸道纤维化中的潜在作用.
- 在喘和肥胖的背景下探索脂肪细胞和纤维细胞之间的相互作用.
- 确定参与脂肪细胞诱导的FMT的分子媒介.
主要方法:
- 在体外共同培养模型中,使用来自有或没有肥胖和喘的患者的脂肪细胞和纤维细胞.
- 蛋白质组分析以确定差异表达的蛋白质.
- 多重分析量化关键信号分子,如TGF-β和素.
主要成果:
- 与肥胖脂肪细胞共同培养的纤维细胞显示纤维素标记物 (α-平滑肌动蛋白,维丁) 的增加,表明FMT.
- 这种FMT效应在喘性纤维细胞中比健康纤维细胞更为明显.
- 肥胖脂肪细胞和喘纤维细胞共同培养显示TGF-β信号通路中的蛋白质升级,同时增加了TGF-β和瘦素的产生.
结论:
- 肥胖脂肪细胞可以促进纤维细胞到肌纤维细胞的过渡,有助于喘中的呼吸道纤维化.
- 转化生长因子-β (TGF-β) 信号通路参与了这个过程.
- 这些发现表明,肥胖与喘严重程度加重和纤维化相关的机制,提供了潜在的治疗点.
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