ArticleBiomolecules2022
RRM2 Alleviates Doxorubicin-Induced Cardiotoxicity through the AKT/mTOR Signaling Pathway.
Article in Biomolecules, 2022. 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.
- FOXA2 enhances anoikis sensitivity in lung adenocarcinoma cells: Dual role of ABCA8 upregulation and NOX4 suppression.Oncology letters · 2026Article
- Autophagic therapeutic targeting for Doxorubicin-induced cardiomyopathy.Molecular biology reports · 2026Review
- CD74 deficiency protects against doxorubicin cardiotoxicity through RRM2-mediated regulation of ferroptosis.Acta pharmaceutica Sinica. B · 2026Article
- Cardiotoxicity induced by traditional chemotherapy: mechanisms and mitigation strategies.Apoptosis : an international journal on programmed cell death · 2026Review
- MCL1 modulates mTORC1 signaling to promote bioenergetics and tumorigenesis.Nature communications · 2025Article
- FEN1 plays a key role in the transition from HSIL to CSCC.Scientific reports · 2025Article
- The mechanism and therapeutic strategies in doxorubicin-induced cardiotoxicity: Role of programmed cell death.Cell stress & chaperones · 2024Review
- Role of gut microbiota in doxorubicin-induced cardiotoxicity: from pathogenesis to related interventions.Journal of translational medicine · 2024Review
- Interferon-regulatory factor-1 boosts bevacizumab cardiotoxicity by the vascular endothelial growth factor A/14-3-3γ axis.ESC heart failure · 2024Article
- The Role of mTOR in Doxorubicin-Altered Cardiac Metabolism: A Promising Therapeutic Target of Natural Compounds.Cardiovascular toxicology · 2024Review
- FUNDC1 alleviates doxorubicin-induced cardiotoxicity by restoring mitochondrial-endoplasmic reticulum contacts and blocked autophagic flux.Theranostics · 2024Article
- IGF2BP3 regulates the expression of RRM2 and promotes the progression of rheumatoid arthritis via RRM2/Akt/MMP-9 pathway.PloS one · 2024Article
- Circular RNA ZBTB46 depletion alleviates the progression of Atherosclerosis by regulating the ubiquitination and degradation of hnRNPA2B1 via the AKT/mTOR pathway.Immunity & ageing : I & A · 2023Article
- Recent Perspectives on Cardiovascular Toxicity Associated with Colorectal Cancer Drug Therapy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Identification of ferroptosis related markers by integrated bioinformatics analysis and In vitro model experiments in rheumatoid arthritis.BMC medical genomics · 2023Article
- Platelet-rich plasma ameliorates lipopolysaccharide-induced cardiac injury by inflammation and ferroptosis regulation.Frontiers in pharmacology · 2022Article
- A new cell-free therapeutic strategy for liver regeneration: Human placental mesenchymal stem cell-derived extracellular vesicles.Journal of tissue engineeringArticle
Corrections and comments
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is an effective chemotherapeutic agent that plays an unparalleled role in cancer treatment. However, its serious dose-dependent cardiotoxicity, which eventually contributes to irreversible heart failure, has greatly limited the widespread clinical application of DOX. A previous study has demonstrated that the ribonucleotide reductase M2 subunit (RRM2) exerts salutary effects on promoting proliferation and inhibiting apoptosis and autophagy. However, the specific function of RRM2 in DOX-induced cardiotoxicity is yet to be determined. This study aimed to elucidate the role and potential mechanism of RRM2 on DOX-induced cardiotoxicity by investigating neonatal primary cardiomyocytes and mice treated with DOX. Subsequently, the results indicated that RRM2 expression was significantly reduced in mice hearts and primary cardiomyocytes. Apoptosis and autophagy-related proteins, such as cleaved-Caspase3 (C-Caspase3), LC3B, and beclin1, were distinctly upregulated. Additionally, RRM2 deficiency led to increased autophagy and apoptosis in cells. RRM2 overexpression, on the contrary, alleviated DOX-induced cardiotoxicity in vivo and in vitro. Consistently, DIDOX, an inhibitor of RRM2, attenuated the protective effect of RRM2. Mechanistically, we found that AKT/mTOR inhibitors could reverse the function of RRM2 overexpression on DOX-induced autophagy and apoptosis, which means that RRM2 could have regulated DOX-induced cardiotoxicity through the AKT/mTOR signaling pathway. In conclusion, our experiment established that RRM2 could be a potential treatment in reversing DOX-induced cardiac dysfunction.
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