ArticleJournal of molecular cell biology2020
Overexpression of mechanical sensitive miR-337-3p alleviates ectopic ossification in rat tendinopathy model via targeting IRS1 and Nox4 of tendon-derived stem cells.
Article in Journal of molecular cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 35 citations in OpenAlex.
- Carnosic acid serves as a dual Nrf2 activator and PTEN/AKT suppressor to inhibit traumatic heterotopic ossification.Stem cell research & therapy · 2025Article
- Leveraging mechanobiology: Identifying mechanotransducers with potential applications for tendon repair.The Journal of physiology · 2025Review
- Targeting miR-337 mitigates disuse-induced bone loss.Cell discovery · 2025Article
- Piezoelectric nanofilms fabricated by coaxial electrospun polycaprolactone/Barium titanate promote Achilles tendon regeneration by reducing IL-17A/NF-κB-mediated inflammation.Bioactive materials · 2025Article
- Exploring molecular and cellular signaling pathways: Unraveling the pathogenesis of tendinopathy.Journal of orthopaedic translation · 2025Review
- Erroneous Differentiation of Tendon Stem/Progenitor Cells in the Pathogenesis of Tendinopathy: Current Evidence and Future Perspectives.Stem cell reviews and reports · 2025Review
- LncRNA CRNDE regulates the differentiation of tendon-derived stem cells and enhances rotator cuff injury repair by modulating the miR-337/TGFBR2 axis.International journal of clinical and experimental pathology · 2025Article
- Tendon Tissue Engineering: Pathophysiological Mechanism and Bioengineering Therapy of Tendinopathy.International journal of nanomedicine · 2025Review
- Mechanosensitive miRNAs in Cartilage and Subchondral Bone Remodeling: Emerging Targets for Osteoarthritis Therapy.Journal of inflammation research · 2025Review
- Tendon mechanobiology in the context of tendon biofabrication.Frontiers in bioengineering and biotechnology · 2025Review
- The role of miRNAs as biomarkers in heterotopic ossification.EFORT open reviews · 2024Review
- Exosomes derived from mir-337-3p over-expressing tendon stem cells protect against apoptosis of tenocytes via targeting caspase3.BMC musculoskeletal disorders · 2024Article
- Oncostatin M promotes osteogenic differentiation of tendon-derived stem cells through the JAK2/STAT3 signalling pathway.Journal of orthopaedic surgery and research · 2024Article
- Circ_0005736 promotes tenogenic differentiation of tendon-derived stem cells through the miR-636/MAPK1 axis.Journal of orthopaedic surgery and research · 2023Article
- MiRNAs as Potential Regulators of Enthesis Healing: Findings in a Rodent Injury Model.International journal of molecular sciences · 2023Article
- Large animal models for the study of tendinopathy.Frontiers in cell and developmental biology · 2022Review
- Differential expression profiles and functional prediction of circRNA in mice with traumatic heterotopic ossification.Frontiers in immunology · 2022Article
- A Hyperglycemic Microenvironment Inhibits Tendon-to-Bone Healing through the let-7b-5p/CFTR Pathway.Computational and mathematical methods in medicine · 2022Article
- Advances in Stem Cell Therapies for Rotator Cuff Injuries.Frontiers in bioengineering and biotechnology · 2022Review
- Characterization of Tendon-Derived Stem Cells and Rescue Tendon Injury.Stem cell reviews and reports · 2021Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tendinopathy, which is characterized by the ectopic ossification of tendon, is a common disease occurring in certain population, such as athletes that suffer from repetitive tendon strains. However, the molecular mechanism underlying the pathogenesis of tendinopathy caused by the overuse of tendon is still lacking. Here, we found that the mechanosensitive miRNA, miR-337-3p, had lower expression under uniaxial cyclical mechanical loading in tendon-derived stem cells (TDSCs) and negatively controlled chondro-osteogenic differentiation of TDSCs. Importantly, downregulation of miR-337-3p expression was also observed in both rat and human calcified tendons, and overexpressing miR-337-3p in patellar tendons of rat tendinopathy model displayed a robust therapeutic efficiency. Mechanistically, we found that the proinflammatory cytokine interleukin-1β was the upstream factor of miR-337-3p that bridges the mechanical loading with its downregulation. Furthermore, the target genes of miR-337-3p, NADPH oxidase 4, and insulin receptor substrate 1, activated chondro-osteogenic differentiation of TDSCs through JNK and ERK signaling, respectively. Thus, these findings not only provide novel insight into the molecular mechanisms underlying ectopic ossification in tendinopathy but also highlight the significance of miR-337-3p as a putative therapeutic target for clinic treatment of tendinopathy.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.