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纤维细胞生长因子18通过调节FOXN2来刺激状细胞的增殖,以减轻创伤后关节炎在小鼠模型中的影响

Zhusong Huang¹, Wenhan Zhao¹, Jinfu Lan¹

¹Department of Orthopedic Surgery, Fuzhou Second General Hospital, Fuzhou, Fujian, China.

Frontiers in bioengineering and biotechnology

|December 1, 2025

概括

纤维细胞生长因子18 (FGF18) 减轻创伤后关节炎 (PTOA),通过降低FOXN2的调节,增强树脂蛋白合成,并抑制软骨降解酶. 在小鼠模型中FGF18的输送减少了PTOA的进展和软骨侵蚀.

科学领域:

生物化学生物化学
分子生物学分子生物学
整形外科整形外科整形外科

背景情况:

骨关节炎 (OA) 的进展与纤维细胞生长因子18 (FGF18) 有关.
在创伤后关节炎 (PTOA) 中,FGF18的特定作用及其与FOXN2的关系尚不清楚.
了解这些分子机制对于开发针对PTOA的向疗法至关重要.

研究的目的:

在PTOA的背景下研究FGF18的表达和功能.
为了探索FGF18和FOXN2在冠状细胞中的相互作用.
在PTOA的小鼠模型中评估FGF18的治疗潜力.

主要方法:

在PTOA患者和正常对照中对关节软骨的基因表达分析进行比较.
试验室功能性测试,以评估FGF18过度表达对状细胞增殖,状细胞合成和软骨降解标记物的影响 (CTX-II,MMP13,ADAMTS-5).
在不稳定的中间半月体 (DMM) 诱导的PTOA小鼠模型中,FGF18的关节内给药.

主要成果:

在PTOA关节软骨中,FGF18表达显著下调.
过度表达FGF18促进了冠状细胞的增殖 (通过BMP2) 和菌素的合成,同时抑制了软骨降解酶 (MMP13,ADAMTS-5) 和CTX-II.
在DMM小鼠中,关节内FGF18的输送减少了软骨侵蚀,突结,并改善了矩阵完整性. FOXN2表达与FGF18水平相反相关.

结论:

通过抑制软骨降解和促进矩阵合成,FGF18在PTOA中起着保护作用.
FGF18针对FOXN2,这表明PTOA的新疗法途径.
这些发现阐明了创伤诱导的软骨病理中的独特分子机制,为PTOA提供了新的治疗策略.

关键词:

第二种类型的原蛋白的C-telopeptide (CTX-II)一种具有血栓丁基因5 (ADAMTS-5) 的分解蛋白和金属蛋白酶.骨形态基因蛋白2 (BMP2) 是一种骨形态基因蛋白.不稳定的中间半月体 (DMM) 模型纤维细胞生长因子18 (FGF18)叉盒 N2 (FOXN2) 的使用情况.创伤后关节炎 (PTOA) 是一种

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