ArticleScientific reports2017
Activation of miR-34a-5p/Sirt1/p66shc pathway contributes to doxorubicin-induced cardiotoxicity.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 95 citations in OpenAlex.
- MicroRNAs and Alarmins in Cardio-Oncology: Biomarkers and Therapeutic Implications in Skin and Breast Cancer.International journal of molecular sciences · 2026Review
- Nutritional Prevention of Oxidative Stress-Induced Cardiotoxicity in Pediatric Cardio-Oncology: Molecular Mechanisms and Translational Perspectives-A Narrative Review.International journal of molecular sciences · 2026Review
- S1UTRSP5, a short restructured RNA from SLIT1 3'UTR, mitigates mouse cardiac remodeling via enhancing SlRT1 activity.Acta pharmacologica Sinica · 2026Article
- MiRNA Regulations in Cardiotoxicity Induced by Oncologic Therapies and Possible Immune Response.Current medicinal chemistry · 2026Review
- Sirtuin 1 is a key molecular link between cellular senescence and heart failure.Frontiers in molecular medicine · 2026Review
- The Role of miRNAs in Chemotherapy-Induced Cardiotoxicity.Biomedicines · 2025Review
- Deciphering the role of crucial miRNAs involved in diabetic cardiomyopathy through a multiomics approach.Scientific reports · 2025Article
- The Role of p66Shc in Cancer: Molecular Mechanisms and Therapeutic Implications.Journal of cellular and molecular medicine · 2025Review
- Non-Coding RNAs in the Regulation of Doxorubicin-Induced Cardiotoxicity.Biomolecules · 2025Review
- Deciphering the roles of cellular and extracellular non-coding RNAs in chemotherapy-induced cardiotoxicity.Molecular and cellular biochemistry · 2025Review
- The role and mechanism of epigenetics in anticancer drug-induced cardiotoxicity.Basic research in cardiology · 2025Review
- MicroRNAs in anthracycline cardiotoxicity: biomarkers, mechanisms, and therapeutic advances.Frontiers in cardiovascular medicine · 2025Review
- Roles of Non-Coding RNA in Anthracycline Cardiotoxicity: A Narrative Review.Journal of inflammation research · 2025Review
- The Role of MicroRNAs in the Pathogenesis of Doxorubicin-Induced Vascular Remodeling.International journal of molecular sciences · 2024Review
- Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Transforming Cardiotoxicity Detection in Cancer Therapies: The Promise of MicroRNAs as Precision Biomarkers.International journal of molecular sciences · 2024Review
- Non-coding RNAs as therapeutic targets and biomarkers in ischaemic heart disease.Nature reviews. Cardiology · 2024Review
- Plasma Extracellular MicroRNAs Associated With Cardiovascular Disease Risk Factors in Middle-Aged and Older Adults.Journal of the American Heart Association · 2024Article
- miRNA Expression Profiles in Isolated Ventricular Cardiomyocytes: Insights into Doxorubicin-Induced Cardiotoxicity.International journal of molecular sciences · 2024Article
- Circulating MicroRNA as Biomarkers of Anthracycline-Induced Cardiotoxicity:JACC. CardioOncology · 2024Review
1 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms underlying anthracyclines-induced cardiotoxicity have not been well elucidated. MiRNAs were revealed dysregulated in the myocardium and plasma of rats received Dox treatment. MicroRNA-34a-5p (miR-34a-5p) was verified increased in the myocardium and plasma of Dox-treated rats, but was reversed in rats received Dox plus DEX treatments. Human miR-34a-5p was also observed increased in the plasma of patients with diffuse large B-cell lymphoma after 9- and 16-week epirubicin therapy. Up-regulation of miR-34a-5p was observed in Dox-induced rat cardiomyocyte H9c2 cells. MiR-34a-5p could augment Bax expression, but inhibited Bcl-2 expression, along with the increases of the activated caspase-3 and mitochondrial potentials in H9C2 cells. MiR-34a-5p was verified to modulate Sirt1 expression post-transcriptionally. In parallel to Sirt1 siRNA, miR-34a-5p could enhance p66shc expression, accompanied by increases of Bax and the activated caspase-3 and a decrease of Bcl-2 in H9c2 cells. Moreover, enforced expression of Sirt1 alleviated Dox-induced apoptosis of H9c2 cells, with suppressing levels of p66shc, Bax, the activated caspase-3 and miR-34a-5p, and enhancing Bcl-2 expression. Therefore, miR-34a-5p enhances cardiomyocyte apoptosis by targeting Sirt1, activation of miR-34a-5p/Sirt1/p66shc pathway contributes to Dox-induced cardiotoxicity, and blockage of this pathway represents a potential cardioprotective effect against anthracyclines.
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