ArticleScientific reports2025
Cardiac shock wave therapy-induced exosome derived from OGD/R-treated H9c2 cells carrying miR-98-5p promote HUVECs angiogenesis.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- From physical impact to biological information flow: shock wave regulation of extracellular vesicles mediated tissue repair.Frontiers in cell and developmental biology · 2026Review
- Extracorporeal shock wave therapy alleviates glucocorticoid-induced injury and dysfunction of bone microvascular endothelial cells via the PI3K/AKT/FOXO1 pathway.Annals of joint · 2026Article
- Recent Advances in Shockwave Therapy for Musculoskeletal and Soft-Tissue Disorders.Life (Basel, Switzerland) · 2025Article
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Authors and funding
6 authors.
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Abstract
Cardiac shock wave therapy (CSWT) as an effectual therapy can activate the function of exosomes to a certain extent. Here, we attempted to examine the role of CSWT in exosome released from ischemic cardiomyocytes and its function in myocardial ischemia recovery. The exosomes derived from OGD/R-treated H9c2 (H9c2-OGD/R-Exo) and CSWT-treated OGD/R-stimulated H9c2 (CSWT-H9c2-OGD/R-Exo) were performed with small RNA sequencing to determine miRNAs that differentially expressed. After miR-98-5p inhibitor transfection, H9c2 were subjected to OGD/R and co-cultured with CSWT-H9c2-OGD/R-Exo, the cell viability, LDH and cell apoptosis were assessed. The transfected HUVECs were co-cultured with CSWT-H9c2-OGD/R-Exo, then HUVECs viability, angiogenesis, migration and invasion were assessed. The luciferase reporter gene assay was conducted to prove the targeting relation between miR-98-5p and FOXN3. miR-98-5p was highly enriched in CSWT-H9c2-OGD/R-Exo in compared with H9c2-OGD/R-Exo. CSWT-H9c2-OGD/R-Exo could improve cell viability, inhibit LDH and cell apoptosis. And miR-98-5p released by CSWT-H9c2-OGD/R-Exo promoted HUVECs viability, angiogenesis, migration and invasion. Further FOXN3 was defined as the downstream target gene of miR-98-5p, and miR-98-5p overexpression decreased FOXN3 expression in HUVECs. Besides, the suppression effects of miR-98-5p inhibitor on HUVECs proliferation, angiogenesis and metastasis was partly blunted by FOXN3 silencing. miR-98-5p released from CSWT-H9c2-OGD/R-Exo promoted HUVECs proliferation, angiogenesis and metastasis through directly targeting and suppressing FOXN3 expression.
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