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该CFP宏分子减弱了衰老的肝脏内内皮细胞驱动的肝星细胞的激活

Guanjie Liu¹, Qingyang Leng¹, Shengda Tian¹

¹Department of Endocrinology, Seventh People's Hospital of Shanghai University of Traditional Chinese Medicine, Shanghai, China.

International journal of biological macromolecules

|February 16, 2026

概括

普罗珀丁 (CFP) 被确定为代谢相关脂肪肝炎 (MASH) 肝纤维化的新生物标志物. 肝脏阴侧内皮细胞 (LSEC) 中减少的CFP与纤维化进展相关,并促进TGF-β1的释放,加剧肝脏损伤.

科学领域:

肝病学肝病学是一种肝病学.
细胞生物学细胞生物学
生物标志物发现发现

背景情况:

代谢相关脂肪肝炎 (MASH) 纤维化是死亡的主要原因.
细胞衰老驱动MASH相关的肝纤维化,但机制尚不清楚.

研究的目的:

确定MASH纤维化新型衰老相关生物标志物.
阐明CFP在MASH相关的肝纤维化中的作用.

主要方法:

临床MASH数据和单细胞衰老概况的综合分析.
权重基因联合表达网络分析 (WGCNA) 和机器学习.
在体内MASH纤维化小鼠模型和体内老化LSEC实验.

主要成果:

普罗珀丁 (CFP) 被确定为老化标志物,在LSEC中表达高,在MASH纤维化中下调.
在MASH纤维化LSEC中减少CFP与减少LYVE1局部化相关.
衰老的LSECs促进了TGF-β1的释放,推动了LX-2细胞的增殖和纤维化.
抑制CFP会加剧衰老和TGF-β1分泌;过度表达CFP会减轻这些影响.

结论:

在MASH中,CFP是细胞衰老和纤维化的关键调节者.
CFP代表了MASH相关的肝纤维化的一个潜在的治疗标.

关键词:

我们的共同渔业政策.细胞衰老细胞衰老肝脏的星状细胞是什么肝脏的鼻状内皮细胞是肝脏内皮细胞.这是一种MASH纤维化.

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