ArticleJournal of inflammation research2024
Macrophage-Myofibroblast Transition as a Potential Origin for Skeletal Muscle Fibrosis After Injury via Complement System Activation.
Article in Journal of inflammation research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- CircSMAD4 shapes matrix-remodeling TAMs in lung adenocarcinoma.Non-coding RNA research · 2026Article
- Macrophage regulation of extracellular matrix remodeling in aging skeletal muscle.Ageing research reviews · 2026Review
- Effect of biodegradable magnesium foil as an anti-adhesion barrier on the healing of rat Achilles tendon.Frontiers in bioengineering and biotechnology · 2026Article
- An Emodin-Depot Microsphere-in-Hydrogel Reprograms the Immuno-myogenic Niche to Enable Volumetric Muscle Loss Repair Revealed by Single-Cell Profiling.Research (Washington, D.C.) · 2026Article
- Repurposed Acarbose Targets Nidogen-1 to Remodel the Tumor Stroma and Suppress Portal Vein Tumor Thrombus in Hepatocellular Carcinoma.Research (Washington, D.C.) · 2026Article
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Quercetin Ameliorates Skeletal Muscle Fibrosis After Injury by Interfering with Macrophage-Myofibroblast Transition.Journal of inflammation research · 2026Article
- UCP2 Upregulates ACSL3 to Enhance Lipid Droplet Release from Acinar Cells and Modulates the Sirt1/Smad3 Pathway to Promote Macrophage-to-Myofibroblast Transition in Chronic Pancreatitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Antioxidant RuCo nanosheet attenuates capsule fibrosis in adhesive capsulitis of shoulder by p38 MAPK signaling pathway inhibition.Materials today. Bio · 2025Article
- Effect of macrophage-to-myofibroblast transition on silicosis.Animal models and experimental medicine · 2025Article
- Black phosphorus-doped silk fibroin coating improves osteogenesis for ameliorative graft-bone healing of polyethylene terephthalate artificial ligaments.Frontiers in bioengineering and biotechnology · 2025Article
- Regenerative potential of immune cells after traumatic muscle injury.Frontiers in immunology · 2025Review
- Stromal cells unifying the pathology of acute and chronic skeletal muscle injury - clue for novel biomaterials.Frontiers in bioengineering and biotechnology · 2025Article
- Macrophage-myofibroblast transition as a novel therapeutic target in shoulder stiffness: multi-omics study and experimental validation.Frontiers in cell and developmental biology · 2025Article
- Si-ITGA6-Loaded Liposomes Inhibit Capsule Fibrosis via the FAK/PI3K/Akt Signaling Pathway in Adhesive Capsulitis of Shoulder.International journal of nanomedicine · 2025Article
- Advances in macrophage-myofibroblast transformation in fibrotic diseases.Frontiers in immunology · 2024Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Acute skeletal muscle injury is common in sports. The injured muscle cannot fully recover due to fibrosis resulting from myofibroblasts. Understanding the origin of fibroblasts is, therefore, important for the development of anti-fibrotic therapies. Accumulating evidence shows that a mechanism called macrophage-myofibroblast transition (MMT) can lead to tissue or organ fibrosis, yet it is still unclear whether MMT exists in skeletal muscle and the exact mechanisms. Methods: Single-cell transcriptome of mice skeletal muscle after acute injury was analyzed with a specific attention on the process of MMT. Cell-cell interaction network, pseudotime trajectory analysis, Gene Ontology (GO), and Kyoto Genome Encyclopedia (KEGG) were conducted. A series of experiments in vivo and in vitro were launched for verification. Results: Single cell transcriptomic analysis indicated that, following acute injury, there were much interactions between macrophages and myofibroblasts. A detailed analysis on macrophages indicated that, CD68 Conclusion: Fibrosis following acute injury is disastrous to skeletal muscle, but the origin of myofibroblasts remains unclear. We proved that, following acute injury, macrophage-myofibroblast transition happened in skeletal muscle, which may contribute to fibrosis formation. This phenomenon mainly occurred at five days post-injury. The complement system can activate MMT. More evidence is needed to directly support the pro-fibrotic role of MMT in skeletal muscle fibrosis after acute injury.
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