ArticleJournal of orthopaedic translation2026
Asymmetrical paravertebral muscles fibrosis causes progression of adolescent idiopathic scoliosis via myostatin signalling in fibro-adipogenic progenitors.
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.
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Who cites it
2 citing papers in PubMed.
- Vitamin E-Related Molecular Signatures in Adolescent Idiopathic Scoliosis: A Hypothesis-Generating Multi-Omics Analysis.Food science & nutrition · 2026Article
- Advancing the continuum of orthopaedic translation: Mechanistic insight, regenerative innovation, and converging technologies.Journal of orthopaedic translation · 2026Article
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9 authors.
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Abstract
Background: Adolescent idiopathic scoliosis (AIS) is characterized by progressive spinal deformity; however, its underlying mechanisms are poorly understood. While asymmetry of the paravertebral muscles (PVMs) has been linked to AIS progression, its molecular basis remains unclear. Methods: PVMs biopsies from the concave and convex sides of 10 patients with AIS (Cobb angle >45°, aged 14-17 years) were collected during corrective surgery for histological and gene expression analyses. Bulk RNA sequencing data (GSE254300) from five paired PVMs samples were reanalysed to identify differentially expressed genes, followed by Gene Ontology enrichment and Gene Set Enrichment Analysis. Single-cell RNA sequencing data (PRJNA722100) were used to examine the pathway activation in fibro-adipogenic progenitors (FAPs). Results: Histological and transcriptomic analyses revealed increased collagen deposition and extracellular matrix (ECM) remodelling on the concave side of PVMs. Single-cell RNA sequencing identified FAPs with enhanced myostatin pathway activation on the concave side of PVMs. Conclusion: This study revealed increased ECM fibrosis was more pronounced on the concave side of PVMs than on the convex side in patients with AIS. Asymmetrical myostatin-driven fibrogenesis in FAPs was a significant mechanism underlying asymmetrical PVMs fibrosis and scoliosis progression, highlighting the therapeutic potential of targeting the myostatin-SMAD3 axis in AIS. The translational potential of this article: This study identified asymmetric, myostatin-driven fibrosis in PVMs as a key contributor to AIS pathogenesis. Therapeutic inhibition of myostatin or SMAD3 significantly reduced spinal deformity and muscle fibrosis in bipedal mouse models, suggesting the potential for using myostatin-targeting agents to slow or prevent scoliosis progression in patients with AIS.
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