ArticleJournal of orthopaedic translation2024
Inhibition of PI3K/AKT signaling pathway prevents blood-induced heterotopic ossification of the injured tendon.
Article in Journal of orthopaedic translation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Comprehensive analysis of mRNA-microRNA-lncRNA expression profiles in post-traumatic elbow heterotopic ossification using RNA sequencing and experimental validation.Annals of medicine · 2026Article
- Metabolic-pathway-based classification of tendinopathy reveals a precise therapeutic strategy targeting chondro-modulatory tenocytes.Bone research · 2026Article
- Tendon stem/progenitor cells in heterotopic ossification: functional regulation, molecular mechanisms and targeted therapeutic strategies.Journal of orthopaedic translation · 2026Review
- Quercetin attenuates tendon stem/progenitor cell senescence and promotes aged tendon repair via AKT/NF-κB/NLRP3-mediated mitophagy activation.Journal of advanced research · 2026Article
- POSTN-Mediated Interplay of M1 Polarized Macrophage with Tendon-Derived Stem Cells to Drive Traumatic Heterotopic Ossification Formation through PTK7/ATK Signaling?Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Regulating inflammation microenvironment and tenogenic differentiation as sequential therapy promotes tendon healing in diabetic rats.Journal of orthopaedic translation · 2025Article
- PI3K-Akt signalling regulates Scx-lineage tenocytes and Tppp3-lineage paratenon sheath cells in neonatal tendon regeneration.Nature communications · 2025Article
- Heterotopic ossification: Current developments and emerging potential therapies.Chinese medical journal · 2025Review
- Advances in osteoarthritis research: From diagnosis, treatment to mechanism studies.Journal of orthopaedic translation · 2024Article
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20 authors.
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Abstract
Objective: It is a common clinical phenomenon that blood infiltrates into the injured tendon caused by sports injuries, accidental injuries, and surgery. However, the role of blood infiltration into the injured tendon has not been investigated. Methods: A blood-induced rat model was established and the impact of blood infiltration on inflammation and HO of the injured tendon was assessed. Cell adhesion, viability, apoptosis, and gene expression were measured to evaluate the effect of blood treatment on tendon stem/progenitor cells (TSPCs). Then RNA-seq was used to assess transcriptomic changes in tendons in a blood infiltration environment. At last, the small molecule drug PI3K inhibitor LY294002 was used for Results: Blood caused acute inflammation in the short term and more severe HO in the long term. Then we found that blood treatment increased cell apoptosis and decreased cell adhesion and tenonic gene expression of TSPCs. Furthermore, blood treatment promoted osteochondrogenic differentiation of TSPCs. Next, we used RNA-seq to find that the PI3K/AKT signaling pathway was activated in blood-treated tendon tissues. By inhibiting PI3K with a small molecule drug LY294002, the expression of osteochondrogenic genes was markedly downregulated while the expression of tenonic genes was significantly upregulated. At last, we also found that LY294002 treatment significantly reduced the tendon HO in the rat blood-induced model. Conclusion: Our findings indicate that the upregulated PI3K/AKT signaling pathway is implicated in the aggravation of tendon HO. Therefore, inhibitors targeting the PI3K/AKT pathway would be a promising approach to treat blood-induced tendon HO.
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