ArticleMolecular medicine reports2020
Cardiac shock wave therapy protects cardiomyocytes from hypoxia‑induced injury by modulating miR‑210.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04694157 (Implication of Cardiac Shock Wave Therapy on Coronary Artery Disease Patients - An Observational Long-term Study), which is not on this map. Cited by 9 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Implication of Cardiac Shock Wave Therapy on Coronary Artery Disease Patients - An Observational Long-term Study
Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Systematic Review on Working Mechanisms of Signaling Pathways in Fibrosis During Shockwave Therapy.International journal of molecular sciences · 2024Pooled it
- A study of extracorporeal cardiac shock wave therapy combined with exercise rehabilitation in postoperative patients with PCI for CHD.Scientific reports · 2025Trial
- Small Extracellular Vesicles in Cardioprotection, Cardiac Repair, and Regeneration: Cargo Mechanisms, Producer Cell Sources, and Translational Development.Biomedicines · 2026Review
- PCSK9 Inhibitor Inclisiran Attenuates Cardiotoxicity Induced by Sequential Anthracycline and Trastuzumab Exposure via NLRP3 and MyD88 Pathway Inhibition.International journal of molecular sciences · 2025Article
- Shock Wave Therapy Alleviates Hypoxia/Reoxygenation-Induced Cardiomyocyte Injury by Inhibiting Both Apoptosis and Ferroptosis.Analytical cellular pathology (Amsterdam) · 2024Article
- Effects of Extracorporeal Shockwave Therapy on Functional Recovery and Circulating miR-375 and miR-382-5p after Subacute and Chronic Spinal Cord Contusion Injury in Rats.Biomedicines · 2022Article
- Article
- Hyperoside protects cardiomyocytes against hypoxia‑induced injury via upregulation of microRNA‑138.Molecular medicine reports · 2021Article
- Hypoxia-Induced miR-210 Overexpression Promotes the Differentiation of Human-Induced Pluripotent Stem Cells to Hepatocyte-Like Cells on Random Nanofiber Poly-L-Lactic Acid/Poly (Oxidative medicine and cellular longevity · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiac shock wave therapy (SWT) has been described as a novel therapeutic strategy that is able to alleviate myocardial ischemic injury. microRNA (miRNA/miR)‑210 plays a cytoprotective role in cardiomyocytes in response to hypoxia by regulating cell apoptosis. The aim of the present study was to investigate whether cardiac SWT could protect cardiomyocytes from hypoxia‑induced injury by regulating miR‑210 expression. The murine adult cardiomyocyte cell line HL‑1 was incubated for 5 h in hypoxic conditions, followed by reoxygenation for 12 h and treatment with SWT immediately following hypoxia in the present study. The cell viability was determined using an MTS assay. Western blot analyses were performed in order to detect cell signaling changes. Reactive oxygen species production was detected using dihydroethidium staining, and malondialdehyde levels were measured using the thiobarbituric acid method. miRNA and mRNA expression levels were confirmed via reverse transcription‑quantitative PCR. Apoptosis was evaluated by means of flow cytometry. HL‑1 cells were then transfected with miR‑210 mimics or inhibitors in order to alter miR‑210 expression levels, and the effects on HL‑1 cells were determined. Hypoxia led to elevated oxidative stress, enhanced cell apoptosis and upregulated miR‑210 expression levels in HL‑1 cells, while SWT could alleviate hypoxia‑induced cell injury and further promote miR‑210 expression. miR‑210 overexpression decreased apoptosis and oxidative stress during hypoxic stress in HL‑1 cells, whereas inhibition of miR‑210 increased cell apoptosis and promoted oxidative stress. Furthermore, miR‑210 inhibition could reverse the effects of SWT on HL‑1 cells. Finally, the mRNA analysis revealed that SWT significantly attenuated apoptosis‑inducing factor mitochondrion‑associated 3 and caspase 8 associated protein 2 mRNA expression levels in cardiomyocytes exposed to hypoxia, which were two targets of miR‑210. SWT could exert cardioprotective effects against hypoxia‑induced cardiac injury by modulating miR‑210.
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Registered trials
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.