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卡斯帕斯-9激活β-catenin信号,促进肺纤维化

Juan Wang^1,2,3, Bei Qing^1,2,3, Linguo Gu^1,2,3

¹Department of Thoracic Surgery, The Second Xiangya Hospital of Central South University, Changsha, China.

Journal of translational medicine

|September 2, 2025

概括

通过增加上皮细胞死亡和激活β-catenin信号,Caspase- 9驱动肺纤维化. 抑制这种Caspase-9/β-catenin通路可能为肺纤维化提供新的治疗方法.

科学领域:

细胞生物学
肺部医学
病理学

背景情况:

肺纤维化 (PF) 是一种进展性肺病,治疗方法有限,其特征是细胞外基质积累和上皮损伤.
膜上皮细胞亡是PF的一个关键特征,但其上游调节者尚未完全理解.
卡斯巴酶-9是亡的启动剂,但其在肺纤维化中的作用需要进一步阐明.

研究的目的:

研究Caspase-9在肺纤维化病变中的作用.
探索Caspase-9有助于肺纤维化的分子机制,包括与β-catenin的相互作用.

主要方法:

在人类PF组织,白素诱导的小鼠模型和TGF-β1治疗的肺上皮细胞中分析了Caspase-9表达.
利用药理抑制,siRNA敲击和Caspase-9的过度表达来评估对纤维化和亡的功能影响.
通过同定位,调节和救援实验检查了Caspase-9和β-catenin之间的相互作用.

主要成果:

在纤维化肺部和TGF-β1刺激细胞中,卡斯巴酶9的调节升高,抑制减少纤维化和亡.
在上皮细胞中减弱TGF-β1诱导的亡和纤维化标志物.
Caspase-9 与β-catenin相互作用,促进其核积累和下游纤维化信号,而β-catenin调节影响纤维化结果.

结论:

通过诱导上皮细胞亡和激活β-catenin信号传递,Caspase- 9促进肺纤维化.
卡斯巴-9/β-catenin轴代表了PF进展的一个关键途径.
针对Caspase-9/β-catenin轴是一个潜在的肺纤维化治疗策略.

关键词:

细胞亡卡斯帕斯9 分裂-卡斯帕-9 肺纤维化维生素B

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