ArticleBritish journal of pharmacology2020
Activation of the MET receptor attenuates doxorubicin-induced cardiotoxicity in vivo and in vitro.
Article in British journal of pharmacology, 2020. 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, 28 citations in OpenAlex.
- Xinmailong Injection Attenuates Doxorubicin-Induced Chronic Heart Failure by Regulating the SIRT1/Caspase-3 Axis and Metabolic Reprogramming: An Integrative Network Pharmacology and Metabolomics Study.Current medical science · 2026Article
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Potential Mechanism by which Eriodictyol Protects against Doxorubicininduced Cardiotoxicity based on Network Pharmacology, Molecular Docking, and Molecular Dynamics Simulation.Current computer-aided drug design · 2025Article
- Vaccarin Ameliorates Doxorubicin-Induced Cardiotoxicity via Inhibition of p38 MAPK Mediated Mitochondrial Dysfunction.Journal of cardiovascular translational research · 2024Article
- Blockage of PHLPP1 protects against myocardial ischemia/reperfusion injury in diabetic mice via activation of STAT3 signaling.Journal of bioenergetics and biomembranes · 2023Article
- Salvianolic Acid B Inhibits Ferroptosis and Apoptosis during Myocardial Ischemia/Reperfusion Injury via Decreasing the Ubiquitin-Proteasome Degradation of GPX4 and the ROS-JNK/MAPK Pathways.Molecules (Basel, Switzerland) · 2023Article
- Paeonol protects against doxorubicin-induced cardiotoxicity by promoting Mfn2-mediated mitochondrial fusion through activating the PKCε-Stat3 pathway.Journal of advanced research · 2023Article
- RGD_PLGA Nanoparticles with Docetaxel: A Route for Improving Drug Efficiency and Reducing Toxicity in Breast Cancer Treatment.Cancers · 2022Article
- RRM2 Alleviates Doxorubicin-Induced Cardiotoxicity through the AKT/mTOR Signaling Pathway.Biomolecules · 2022Article
- IL-17A Increases Doxorubicin Efficacy in Triple Negative Breast Cancer.Frontiers in oncology · 2022Article
- Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Evaluation of the Effect of Crocin on Doxorubicin-Induced Cardiotoxicity.Advances in experimental medicine and biology · 2021Article
- Engineering, Characterization, and Biological Evaluation of an Antibody Targeting the HGF Receptor.Frontiers in immunology · 2021Article
- Interleukin-22 deficiency alleviates doxorubicin-induced oxidative stress and cardiac injury via the p38 MAPK/macrophage/Fizz3 axis in mice.Redox biology · 2020Article
- Therapeutic implications of the PP2A/MET signalling axis in doxorubicin-induced cardiotoxicity and antitumour properties.British journal of pharmacology · 2020Article
- The Long-Lasting Protective Effect of HGF in Cardiomyoblasts Exposed to Doxorubicin Requires a Positive Feed-Forward Loop Mediated by Erk1,2-Timp1-Stat3.International journal of molecular sciences · 2020Article
- Activation of the MET receptor attenuates doxorubicin-induced cardiotoxicity in vivo and in vitro.British journal of pharmacology · 2020Article
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12 authors at 2 institutions in 1 country.
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Abstract
background and purposeDoxorubicin anti-cancer therapy is associated with cardiotoxicity, resulting from DNA damage response (DDR). Hepatocyte growth factor (HGF) protects cardiomyocytes from injury, but its effective use is compromised by low biodistribution. In this study, we have investigated whether the activation of the HGF receptor-encoded by the Met gene-by an agonist monoclonal antibody (mAb) could protect against doxorubicin-induced cardiotoxicity. EXPERIMENTAL APPROACH: The mAb (5 mg·kg KEY
resultsIn vivo, administration of the mAb alleviated doxorubicin-induced cardiac dysfunction and fibrosis. In vitro, mAb mimicked the response to HGF by (a) inhibiting histone H2AX phosphorylation at S139, (b) quenching the expression of the DNA repair enzyme PARP1, and (c) reducing the proteolytic activation of caspase 3. The MET-driven cardioprotection involved, at least in vitro, the phosphorylation of STAT3. CONCLUSION AND IMPLICATIONS: The MET agonist mAb provides a new tool for cardioprotection against anthracycline cardiotoxicity.
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