ArticleEMBO molecular medicine2023
Combinatorial activation of the WNT-dependent fibrogenic program by distinct complement subunits in dystrophic muscle.
Article in EMBO molecular medicine, 2023. 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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Who cites it
10 citing papers in PubMed, 10 citations in OpenAlex.
- Mesenchymal Stromal Cell-Mediated Intercellular Communication: Mapping the Interactome for Skeletal Muscle Homeostasis and Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Identification of myokines associated with the pathological stress response in theJournal of neuromuscular diseases · 2026Article
- The Role of Fibro/adipogenic Progenitors (FAPs) in Sarcopenia: Mechanisms and Potential Therapeutic Strategies.Stem cell reviews and reports · 2026Review
- Impact of C4BPA on Muscle progenitor cell differentiation: insights for Duchenne muscular dystrophy treatment.Cell death & disease · 2026Article
- Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Persistent tissue regeneration and transforming growth factor-β induced fibrosis in the masseter muscle of mdxScientific reports · 2025Article
- Nanomaterial-Mediated Reprogramming of Macrophages to Inhibit Refractory Muscle Fibrosis.Advanced materials (Deerfield Beach, Fla.) · 2024Article
- Proteomic profiling of human plasma extracellular vesicles identifies PF4 and C1R as novel biomarker in sarcopenia.Journal of cachexia, sarcopenia and muscle · 2024Article
- Combinatorial activation of the WNT-dependent fibrogenic program by distinct complement subunits in dystrophic muscle.EMBO molecular medicine · 2023Article
- Exploring the therapeutic potential of fibroadipogenic progenitors in muscle disease.Journal of neuromuscular diseasesReview
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Authors and funding
9 authors at 3 institutions in 2 countries.
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Abstract
Fibrosis is associated with compromised muscle functionality in Duchenne muscular dystrophy (DMD). We report observations with tissues from dystrophic patients and mice supporting a model to explain fibrosis in DMD, which relies on the crosstalk between the complement and the WNT signaling pathways and the functional interactions of two cellular types. Fibro-adipogenic progenitors and macrophages, which populate the inflamed dystrophic muscles, act as a combinatorial source of WNT activity by secreting distinct subunits of the C1 complement complex. The resulting aberrant activation of the WNT signaling in responsive cells, such as fibro-adipogenic progenitors, contributes to fibrosis. Indeed, pharmacological inhibition of the C1r/s subunits in a murine model of DMD mitigated the activation of the WNT signaling pathway, reduced the fibrogenic characteristics of the fibro-adipogenic progenitors, and ameliorated the dystrophic phenotype. These studies shed new light on the molecular and cellular mechanisms responsible for fibrosis in muscular dystrophy and open to new therapeutic strategies.
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