ArticleMolecular therapy. Nucleic acids2018
miR-24 and miR-122 Negatively Regulate the Transforming Growth Factor-β/Smad Signaling Pathway in Skeletal Muscle Fibrosis.
Article in Molecular therapy. Nucleic acids, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 106 citations in OpenAlex.
- RNA Chemical Modifications in Mammalian Skeletal Muscle Development, Homeostasis, and Disease: Regulatory Mechanisms and Chemical Biology Perspectives.Molecules (Basel, Switzerland) · 2026Review
- MicroRNA Crosstalk in Metabolic Disorders: The Dual Role of miR-122 and miR-34a in NAFLD and Type 2 Diabetes.Molecular biotechnology · 2026Review
- Pulmonary responses to polyacrylic acid with and without carboxyl groups following intratracheal instillation in rats.Archives of toxicology · 2026Article
- Myofibroblast lineage mapping and inhibiting subretinal fibrosis by targeting SMAD3 and MRTF pathways via microRNA-24 functional study.bioRxiv : the preprint server for biology · 2026Article
- Signaling pathway networks in frozen shoulder fibrosis: from inflammatory initiation to fibrotic progression.Frontiers in medicine · 2026Review
- Molecular mechanisms of skeletal muscle fibrosis and potential targeted therapeutic strategies.Frontiers in immunology · 2026Review
- RUNX1-mediated repression of miR-24 promotes hepatic stellate cell activation and liver fibrosis by targeting the ALK4/Smad3 signaling pathway.Frontiers in genetics · 2026Article
- Exosomal miR-122-5p from tubular cells ameliorates renal interstitial fibrosis by regulating fibroblasts via HIF-1α.Cell death discovery · 2025Article
- MyomiRs Expression in Limb Girdle Muscular Dystrophy.IUBMB life · 2025Review
- Liposome-Enabled Nanomaterials for Muscle Regeneration.Small methods · 2025Review
- Leptin Enhances M1 Macrophage Polarization and Impairs Tendon-Bone Healing in Rotator Cuff Repair: A Rat Model.Clinical orthopaedics and related research · 2025Article
- Bio-loggers and miRNAs are innovative tools for measuring physiological changes in lambs during transport.Journal of animal science · 2025Article
- Hepatic miR-149-5p upregulation fosters steatosis, inflammation and fibrosis development in mice and in human liver organoids.JHEP reports : innovation in hepatology · 2024Article
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- Serum miR‑29 is increased in mice with early liver fibrosis.Experimental and therapeutic medicine · 2024Article
- Agomir-122-loaded nanoparticles coated with cell membrane of activated fibroblasts to treat frozen shoulder based on homologous targeting.Journal of nanobiotechnology · 2024Article
- MicroRNA-542-3p targets Pten to inhibit the myoblasts proliferation but suppresses myogenic differentiation independent of targeted Pten.BMC genomics · 2024Article
- Low-intensity pulsed ultrasound reduces alveolar bone resorption during orthodontic treatmentWorld journal of stem cells · 2024Article
- Fibroblast-derived extracellular vesicles as trackable efficient transporters of an experimental nanodrug with fibrotic heart and lung targeting.Theranostics · 2024Article
- Regulation of ferroptosis in osteoarthritis and osteoarthritic chondrocytes by typical MicroRNAs in chondrocytes.Frontiers in medicine · 2024Review
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrosis is common after skeletal muscle injury, undermining tissue regeneration and function. The mechanism underlying skeletal muscle fibrosis remains unveiled. Transforming growth factor-β/Smad signaling pathway is supposed to play a pivotal role. However, how microRNAs interact with transforming growth factor-β/Smad-related muscle fibrosis remains unclear. We showed that microRNA (miR)-24-3p and miR-122-5p declined in skeletal muscle fibrosis, which was a consequence of transforming growth factor-β. Upregulating Smad4 suppressed two microRNAs, whereas inhibiting Smad4 elevated microRNAs. Luciferase reporter assay and chromatin immunoprecipitation confirmed that Smad4 directly inhibited two microRNAs. On the other hand, overexpression of these two miRs retarded fibrotic process. We further identified that Smad2 was a direct target of miR-24-3p, whereas miR-122-5p targeted transforming growth factor-β receptor-II. Both targets were important participants in transforming growth factor-β/Smad signaling. Taken together, a positive feedback loop in transforming growth factor-β/Smad4 signaling pathway in skeletal muscle fibrosis was identified. Transforming growth factor-β/Smad axis could be downregulated by microRNAs. This effect, however, was suppressed by Smad4, the downstream of transforming growth factor-β.
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