ArticleJournal of orthopaedic surgery and research2024
miR-27b-3p reduces muscle fibrosis during chronic skeletal muscle injury by targeting TGF-βR1/Smad pathway.
Article in Journal of orthopaedic surgery and research, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Review
- RNA cargo profiling of muscle extracellular vesicles identifies candidate biomarkers of disease activity and muscle degeneration in FSHD.Journal of translational medicine · 2026Article
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Mechanistic effects of percutaneous needle fasciotomy combined with stretching on early-stage skeletal muscle fibrosis in rats: focus on the TGF-β1/Smad signaling pathway.Journal of orthopaedic surgery and research · 2025Article
- MyomiRs Expression in Limb Girdle Muscular Dystrophy.IUBMB life · 2025Review
- miR-27b-3p modulates liver sinusoidal endothelium dedifferentiation in chronic liver disease.Hepatology communications · 2025Article
- Characterization of rectus femoris lesions in knee osteoarthritis at different stages and the effect of ultrasound-guided acupotomy.Frontiers in physiology · 2024Article
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Authors and funding
6 authors.
Funding
Abstract
backgroundFibrosis is a significant pathological feature of chronic skeletal muscle injury, profoundly affecting muscle regeneration. Fibro-adipogenic progenitors (FAPs) have the ability to differentiate into myofibroblasts, acting as a primary source of extracellular matrix (ECM). the process by which FAPs differentiate into myofibroblasts during chronic skeletal muscle injury remains inadequately explored.
methodmouse model with sciatic nerve denervated was constructed and miRNA expression profiles between the mouse model and uninjured mouse were analyzed. qRT/PCR and immunofluorescence elucidated the effect of miR-27b-3p on fibrosis in vivo and in vitro. Dual-luciferase reporter identified the target gene of miR-27b-3p, and finally knocked down or overexpressed the target gene and phosphorylation inhibition of Smad verified the influence of downstream molecules on the abundance of miR-27b-3p and fibrogenic differentiation of FAPs.
resultFAPs derived from a mouse model with sciatic nerves denervated exhibited a progressively worsening fibrotic phenotype over time. Introducing agomiR-27b-3p effectively suppressed fibrosis both in vitro and in vivo. MiR-27b-3p targeted Transforming Growth Factor Beta Receptor 1 (TGF-βR1) and the abundance of miR-27b-3p was negatively regulated by TGF-βR1/Smad.
conclusionmiR-27b-3p targeting the TGF-βR1/Smad pathway is a novel mechanism for regulating fibrogenic differentiation of FAPs. Increasing abundance of miR-27b-3p, suppressing expression of TGF-βR1 and inhibiting phosphorylation of smad3 presented potential strategies for treating fibrosis in chronic skeletal muscle injury.
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