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纤维细胞生长因子9激活纤维细胞激活,并驱动肩部硬的进展

Jian Xu¹, Weihan Yu², Yunkang Kang¹

¹Department of Orthopaedics, Sports Medicine and Arthroscopy, Fuyang People's Hospital Affiliated to Anhui Medical University, Fuyang, Anhui, China.

Frontiers in cell and developmental biology

|January 15, 2026

概括

纤维细胞生长因子9 (FGF9) 通过PI3K/Akt通路促进关节囊纤维化,导致肩部硬. 抑制这种途径为SS提供了一个潜在的治疗策略.

科学领域:

整形外科整形外科整形外科
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

肩部硬 (SS) 的特点是疼痛和有限的运动范围 (ROM),源于突炎和关节囊纤维化.
导致SS病变的精确分子机制在很大程度上是未知的.
这项研究的重点是确定关节囊纤维化SS.关节囊纤维化的关键分子驱动因素.

研究的目的:

调查推动关节囊纤维化在肩部硬 (SS) 的分子机制.
为了确定参与SS病变的关键分子参与者.
评估针对SS中已识别的途径的治疗潜力.

主要方法:

来自SS和非SS患者的关节囊样本的高通量RNA测序和生物信息分析.
通过关节固定来建立SS的小鼠模型.
采用NIH3T3纤维细胞的体外研究和体内研究涉及小鼠SS模型中的关节内注射,使用LY294002作为PI3K/Akt抑制剂.

主要成果:

转录组分析揭示了100个差异表达基因 (DEGs),纤维细胞生长因子9 (FGF9) 被确定为SS囊中的关键上调基因.
在体外,FGF9增强了NIH3T3细胞迁移,增殖和α-SMA表达,其影响被LY294002.2减轻.
在体内,LY294002治疗减少了SS小鼠的关节囊加厚,纤维化,并改善了SS小鼠的被动ROM.

结论:

在SS中,FGF9通过激活PI3K/Akt信号通路来促进纤维细胞激活和关节囊纤维化.
针对PI3K/Akt信号通路的向抑制为肩部硬提供了一个有希望的治疗途径.
了解FGF9介导的PI3K/Akt通路对于开发新型SS治疗至关重要.

关键词:

FGF9 联邦政府财政基金在PI3K/AKT中使用.纤维化纤维化肩膀硬肩膀硬肩膀硬肩膀硬转录组学转录组学是指转录组学.

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