ArticleNature communications2025
Epitenon-derived progenitors drive fibrosis and regeneration after flexor tendon injury in a spatially-dependent manner.
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 10 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
10 citing papers in PubMed.
- Creb3l1 Overexpression Improves Flexor Tendon Repair in Aged Rats.Aging cell · 2026Article
- A human synovial tendon-on-a-chip models key features of peritendinous adhesions and offers a new approach methodology for testing anti-fibrotic drugs.bioRxiv : the preprint server for biology · 2026Article
- The cellular basis of fibrotic tendon healing: now in higher definition.American journal of physiology. Cell physiology · 2026Review
- Recapitulating the Native Tendon Environment in a Synthetic 3D Anisotropic Hydrogel as an Engineered Extracellular Matrix.ACS applied bio materials · 2026Article
- Single-cell transcriptional mapping ofJBMR plus · 2026Article
- Effect of Vitamin C Injection on Flexor Tendon Healing in Zone II: A Randomized Controlled Trial.Cureus · 2026Article
- Nociceptive sensory neuron-derived NGF orchestrates a fibrotic mesenchymal stromal cell neurogenic niche to drive tendon pathological fibrosis.Nature communications · 2025Article
- Article
- A Healing Tendon-cy: Organized research in tenocyte biology and bio-resorbable grafts for tendon rupture recovery.Data in brief · 2025Article
- Single-cell sequencing reveals cellular heterogeneity and molecular mechanisms in tendon and enthesis injury repair.Frontiers in physiology · 2025Review
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7 authors.
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Abstract
Flexor tendon injuries are common and heal poorly owing to both the deposition of function-limiting peritendinous scar tissue and insufficient healing of the tendon itself. Therapeutic options are limited due to a lack of understanding of the cell populations that contribute to these processes. Here, we identified the epitenon as a major source of cells that contribute to both peritendinous fibrosis and regenerative tendon healing following acute tendon injury. Using a combination of genetic lineage tracing and single cell RNA-sequencing (scRNA-seq), we profiled the behavior and contributions of each cell fate to the healing process in a spatio-temporal manner. Integrated scRNA-seq analysis of mouse healing with human peritendinous scar tissue revealed remarkable transcriptional similarity between mouse epitenon-derived cells and fibroblasts present in human peritendinous scar tissue, which was further validated by immunofluorescent staining for conserved markers. Finally, ablation of pro-fibrotic epitenon-derived cells post-tendon injury significantly improved functional recovery. Combined, these results clearly identify the epitenon as the cellular origin of an important progenitor cell population that could be leveraged to improve tendon healing.
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