ArticleBritish journal of pharmacology2017
Signalling mechanisms underlying doxorubicin and Nox2 NADPH oxidase-induced cardiomyopathy: involvement of mitofusin-2.
Article in British journal of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 52 citations in OpenAlex.
- Doxorubicin-Induced Cardiac Remodeling: Mechanisms and Mitigation Strategies.Cardiovascular drugs and therapy · 2026Review
- Understanding the Mechanisms of Chemotherapy-Related Cardiotoxicity Employing hiPSC-Derived Cardiomyocyte Models for Drug Screening and the Identification of Genetic and Epigenetic Variants.International journal of molecular sciences · 2025Review
- NADPH Oxidases in Cancer Therapy-Induced Cardiotoxicity: Mechanisms and Therapeutic Approaches.Cardiovascular toxicology · 2025Review
- Losmapimod ameliorates doxorubicin-induced cardiotoxicity through attenuating senescence and inflammatory pathways.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Food therapy of scutellarein ameliorates pirarubicin‑induced cardiotoxicity in rats by inhibiting apoptosis and ferroptosis through regulation of NOX2‑induced oxidative stress.Molecular medicine reports · 2024Article
- NADPH oxidase 2 mediates cardiac sympathetic denervation and myocyte autophagy, resulting in cardiac atrophy and dysfunction in doxorubicin-induced cardiomyopathy.Scientific reports · 2024Article
- The Association between NADPH Oxidase 2 (NOX2) and Drug Resistance in Cancer.Current cancer drug targets · 2024Review
- Review on the protective mechanism of astragaloside IV against cardiovascular diseases.Frontiers in pharmacology · 2023Review
- The beneficial role of exercise in preventing doxorubicin-induced cardiotoxicity.Frontiers in physiology · 2023Review
- Anthracycline-induced cardiotoxicity and cell senescence: new therapeutic option?Cellular and molecular life sciences : CMLS · 2022Review
- Therapeutic Targets for DOX-Induced Cardiomyopathy: Role of Apoptosis vs. Ferroptosis.International journal of molecular sciences · 2022Review
- High Sensitivity Troponin T as Complementary Modality for Determining Doxorubicin Regimen Cardiotoxicity in Non-Hodgkin Lymphoma Patients.Advanced pharmaceutical bulletin · 2022Article
- Underlying the Mechanisms of Doxorubicin-Induced Acute Cardiotoxicity: Oxidative Stress and Cell Death.International journal of biological sciences · 2022Review
- Therapeutic Potential of Astragaloside IV Against Adriamycin-Induced Renal Damage in RatsFrontiers in pharmacology · 2022Article
- Setanaxib (GKT137831) Ameliorates Doxorubicin-Induced Cardiotoxicity by Inhibiting the NOX1/NOX4/Reactive Oxygen Species/MAPK Pathway.Frontiers in pharmacology · 2022Article
- Molecular mechanisms associated with the chemoprotective role of protocatechuic acid and its potential benefits in the amelioration of doxorubicin-induced cardiotoxicity: A review.Toxicology reports · 2022Review
- Long-Chain and Very Long-Chain Ceramides Mediate Doxorubicin-Induced Toxicity and Fibrosis.International journal of molecular sciences · 2021Article
- Anticancer Drug-Induced Cardiotoxicity: Insights and Pharmacogenetics.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Chronic exposure to tramadol induces cardiac inflammation and endothelial dysfunction in mice.Scientific reports · 2021Article
- Anthracyclines Suppress Both NADPH Oxidase- Dependent and -Independent NETosis in Human Neutrophils.Cancers · 2019Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
background and purposeThe anthracycline doxorubicin (DOX), although successful as a first-line cancer treatment, induces cardiotoxicity linked with increased production of myocardial ROS, with Nox2 NADPH oxidase-derived superoxide reported to play a key role. The aim of this study was to identify novel mechanisms underlying development of cardiac remodelling/dysfunction further to DOX-stimulated Nox2 activation. EXPERIMENTAL APPROACH: Nox2 KEY
resultsDOX-induced cardiac dysfunction, cardiomyocyte remodelling, superoxide production and apoptosis in WT mice were attenuated in Nox2 CONCLUSIONS AND IMPLICATIONS: DOX-induced and Nox2-mediated up-regulation of Mfn2, rather than contributing to cardiomyocyte dysfunction through apoptotic pathways, appears to promote a protective mechanism. LINKED ARTICLES: This article is part of a themed section on New Insights into Cardiotoxicity Caused by Chemotherapeutic Agents. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v174.21/issuetoc.
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