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衰老的肺中介质干细胞通过FGF-4/FOXM1轴驱动肺纤维化

Yuxin Liu^1,2, Jie Ji^1,2, Shudan Zheng^1,2

¹State Key Laboratory of Analytical Chemistry for Life Science, Division of Anatomy and Histo-embryology, Medical School, Nanjing University, Nanjing, Jiangsu, 210093, China.

Stem cell research & therapy

|September 17, 2024

概括

细胞衰老驱动异常性肺纤维化 (IPF). 纤维细胞生长因子4 (FGF-4) 来自老化的介质干细胞 (MSCs) 通过通过FOXM1.1.激活Wnt信号来促进纤维化. 阻断这个轴可以治疗IPF.

科学领域:

肺部医学肺部医学
细胞生物学细胞生物学
纤维化研究纤维化研究

背景情况:

异常性肺纤维化 (IPF) 是一种与年龄相关的肺部疾病,其特征是异常的痕和肺功能减弱.
细胞衰老越来越被认为是IPF病变发生的关键驱动因素.
了解IPF进展的分子机制对于开发向疗法至关重要.

研究的目的:

调查细胞衰老在IPF中的作用.
为了确定参与衰老细胞介导的肺纤维化中的分子途径.
探索IPF的潜在治疗点.

主要方法:

在小鼠中诱导肺纤维化,使用白素.
通过免疫光对细胞衰老的评估.
评估纤维细胞生长因子4 (FGF-4) 对纤维细胞激活的影响,使用西布洛特和qPCR.
对Wnt信号和FOXM1参与的分析.

主要成果:

衰老的介质干细胞 (MSC) 在IPF肺部升高,与纤维化严重程度相关.
衰老的MSCs在体外和体内都会诱导肺纤维化表型.
在衰老的MSC中FGF-4的升高通过Wnt信号以FOXM1-依赖的方式激活肺纤维细胞.
用斯特抑制FOXM1的抑制抑制了FGF-4诱导的纤维细胞激活和肺纤维化.

结论:

FGF-4是衰老的MSC驱动的肺纤维化中的关键调解者.
针对衰老的MSC或FGF-4/FOXM1信号通路,为IPF提供了一个有前途的治疗策略.
对老化剂和FGF-4/FOXM1抑制剂的进一步研究可能会导致有效的IPF治疗方法.

关键词:

细胞衰老细胞衰老在FGF-4中.在FOXM1上.异形性肺纤维化症异形性肺纤维化症介质细胞干细胞介质细胞干细胞

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