ArticleJournal of orthopaedic translation2026
Profibrotic macrophage-derived CXCL4 promotes pericyte-to-myofibroblast transition after spinal cord injury.
Article in Journal of orthopaedic translation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
2 citing papers in PubMed.
- Review
- Advancing the continuum of orthopaedic translation: Mechanistic insight, regenerative innovation, and converging technologies.Journal of orthopaedic translation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Spinal cord injury (SCI) induces fibrotic scarring that impairs axonal regeneration. Pericytes contribute to scar formation via pericyte-to-myofibroblast transition (PMT), yet the mechanisms underlying PMT in SCI remain unclear. Although CXCL4, a pleiotropic chemokine, is implicated in various fibrotic disorders, its role in driving PMT post-SCI remains unexplored. Objectives: To investigate whether CXCL4 drives PMT after SCI, elucidate its mechanisms, and assess its therapeutic potential. Methods: scRNA-seq characterized cell-type dynamics and profibrotic signals in injured mouse spinal cords. Results: PMT occurred post SCI, with Pdgfrβ Conclusion: Profibrotic macrophage-derived CXCL4 activates CXCR3/PI3K/Akt signaling in pericytes, driving their transition into scar-forming myofibroblasts after SCI. Blocking this axis mitigates fibrosis and enhances axonal regeneration and motor recovery. The translational potential of this article: This study indicates that targeting the CXCL4-driven pericyte-to-myofibroblast transition to reduce fibrotic scar formation may provide an effective therapeutic strategy for enhancing axonal regeneration and functional recovery after SCI.
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Registered trials
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