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<p>Tissue fibrosis is a major cause of organ dysfunction. Preventing fibrosis in tissue pathological condition remains a significant clinical challenge. Here we investigate the role of fibroblast growth factor 7 (FGF7) in mitigating fibrosis and promoting regeneration of load-bearing tendons. Fgf7 knockout mice exhibit impaired motor function and disordered matrix assembly in tendons. Single-cell RNA sequencing reveals an enrichment of a pro-fibrotic cell subpopulation in Fgf7-deficient tendons, which is also predominant in human tendinopathy. Using ProTracer technology, we find that FGF7 deficiency drives proliferating cells toward this pro-fibrotic lineage. Furthermore, we find that FGF7 promotes the tenogenic differentiation of tendon stem/progenitor cells while suppressing their fibrotic differentiation. Importantly, a hydrogel loaded with recombinant FGF7 effectively reduces fibrosis and significantly promotes functional tendon regeneration in vivo. These findings elucidate FGF7’s dual role in driving tenogenesis and inhibiting fibrosis, suggesting a potential therapeutic strategy.</p>

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FGF7 promotes load-bearing tendon regeneration and suppresses fibrosis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年12月27日

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  • Ruifu Lin,
  • Junchao Luo,
  • Hong Zhang,
  • Chunmei Fan,
  • Yue Hu,
  • Ruojin Yan,
  • Zetao Wang,
  • Yang Fei,
  • Chenqi Tang,
  • Tianxi Huang,
  • Tianshun Fang,
  • Weiliang Shen,
  • Sunbin Ling,
  • Hongwei Ouyang,
  • Xiao Chen,
  • Zi Yin

摘要

Tissue fibrosis is a major cause of organ dysfunction. Preventing fibrosis in tissue pathological condition remains a significant clinical challenge. Here we investigate the role of fibroblast growth factor 7 (FGF7) in mitigating fibrosis and promoting regeneration of load-bearing tendons. Fgf7 knockout mice exhibit impaired motor function and disordered matrix assembly in tendons. Single-cell RNA sequencing reveals an enrichment of a pro-fibrotic cell subpopulation in Fgf7-deficient tendons, which is also predominant in human tendinopathy. Using ProTracer technology, we find that FGF7 deficiency drives proliferating cells toward this pro-fibrotic lineage. Furthermore, we find that FGF7 promotes the tenogenic differentiation of tendon stem/progenitor cells while suppressing their fibrotic differentiation. Importantly, a hydrogel loaded with recombinant FGF7 effectively reduces fibrosis and significantly promotes functional tendon regeneration in vivo. These findings elucidate FGF7’s dual role in driving tenogenesis and inhibiting fibrosis, suggesting a potential therapeutic strategy.