ArticleNature communications2025
FGF7 promotes load-bearing tendon regeneration and suppresses fibrosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Metabolic-pathway-based classification of tendinopathy reveals a precise therapeutic strategy targeting chondro-modulatory tenocytes.Bone research · 2026Article
- Fibroblast Growth Factor 7 Limits Fibroblast-Driven Matrix Remodeling in Abdominal Aortic Aneurysm.Cardiovascular drugs and therapy · 2026Article
- FGF family in health and disease.Molecular biomedicine · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
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