ArticleJournal of cellular physiology2018
Protective effect of miR378* on doxorubicin-induced cardiomyocyte injury via calumenin.
Article in Journal of cellular physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Mechanism of myocardial damage induced by doxorubicinWorld journal of cardiology · 2025Article
- Endoplasmic reticulum stress in cardiomyopathies: from the unfolded protein response to therapeutic opportunities.Frontiers in cardiovascular medicine · 2025Review
- Human neural stem cell secretome relieves endoplasmic reticulum stress-induced apoptosis and improves neuronal functions after traumatic brain injury in a rat model.Journal of molecular histology · 2024Article
- Exercise Attenuates Doxorubicin-Induced Myocardial Injury by Inhibiting TSHR and Regulating Macrophage Polarization Through miR-30d-5p/GALNT7.Journal of immunology research · 2024Article
- Potential role of endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity-an update.Frontiers in pharmacology · 2024Review
- MicroRNA‑378: An important player in cardiovascular diseases (Review).Molecular medicine reports · 2023Review
- Article
- Non-coding RNAs in cancer therapy-induced cardiotoxicity: Mechanisms, biomarkers, and treatments.Frontiers in cardiovascular medicine · 2022Review
- Recent Advances in Gene Therapy for Cardiac Tissue Regeneration.International journal of molecular sciences · 2021Review
- S100A6, Calumenin and Cytohesin 2 as Biomarkers for Cutaneous Involvement in Systemic Sclerosis Patients: A Case Control Study.Journal of personalized medicine · 2021Article
- Hydrogen sulfide ameliorates doxorubicin‑induced myocardial fibrosis in rats via the PI3K/AKT/mTOR pathway.Molecular medicine reports · 2021Article
- MicroRNAs as Biomarkers and Therapeutic Targets in Doxorubicin-Induced Cardiomyopathy: A Review.Frontiers in cardiovascular medicine · 2021Review
- Calumenin contributes to epithelial-mesenchymal transition and predicts poor survival in glioma.Translational neuroscience · 2021Article
- Gene therapy for cardiovascular diseases in China: basic research.Gene therapy · 2020Review
- Protective Effect of miR-204 on Doxorubicin-Induced Cardiomyocyte Injury via HMGB1.Oxidative medicine and cellular longevity · 2020Article
- miR-34b/c regulates doxorubicin-induced myocardial cell injury through ITCH.Cell cycle (Georgetown, Tex.) · 2019Article
- Protective effect of miR378* on doxorubicin-induced cardiomyocyte injury via calumenin.Journal of cellular physiology · 2018Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (Dox) is a highly effective antitumor antibiotic, however myocardial toxicity severely limits its use clinically. The pathogenesis of doxorubicin-induced cardiomyopathy is unclear. In Dox cardiomyopathy mice, there is a decline in cardiac function, a change in myocardial pathology and a reduction in miR378* expression. Expression changes in calumenin, an endoplasmic reticulum stress (ERS) chaperone protein and pathway factor, as well as apoptosis, were observed in cardiomyocytes after doxorubicin-induced injury. However, miR378* increased calumenin expression, eased ERS, and reduced cardiomyocyte apoptosis, while, silencing miR378* reduced calumenin expression, aggravated ERS, and increased cardiomyocyte apoptosis. The above results indicate that miR378* alleviates ERS and inhibits the activation of the ERS-mediated apoptosis signaling pathway in cardiomyocytes via regulating calumenin expression, thereby reducing cardiomyocyte apoptosis after doxorubicin-induced injury. Increasing miR378* expression may be a new way to improve cardiac function and quality of life in patients with Dox cardiomyopathy.
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Registered trials
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