ArticleFrontiers in pharmacology2020
New Insights About Doxorubicin-Induced Toxicity to Cardiomyoblast-Derived H9C2 Cells and Dexrazoxane Cytoprotective Effect: Contribution of
Article in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 43 citations in OpenAlex.
- In Silico, In Vitro, and In Vivo Evaluation of Woodfordia Fruticosa for Cardio Protection against Doxorubicin-Induced Cardiomyopathy.Chemistry & biodiversity · 2026Article
- 14,15-Dihydroxyeicosatrienoic acid, a soluble epoxide hydrolase metabolite in blood, is a predictor of anthracycline-induced cardiotoxicity - a hypothesis generating study.Cardio-oncology (London, England) · 2023Article
- Lactate Can Modulate the Antineoplastic Effects of Doxorubicin and Relieve the Drug's Oxidative Damage on Cardiomyocytes.Cancers · 2023Article
- In vitro to clinical translational pharmacokinetic/pharmacodynamic modeling of doxorubicin (DOX) and dexrazoxane (DEX) interactions: Safety assessment and optimization.Scientific reports · 2023Article
- Protective effect of cafestol against doxorubicin-induced cardiotoxicity in rats by activating the Nrf2 pathway.Frontiers in pharmacology · 2023Article
- Magnesium hexacyanoferrate nanocatalysts attenuate chemodrug-induced cardiotoxicity through an anti-apoptosis mechanism driven by modulation of ferrous iron.Nature communications · 2022Article
- Exogenous 8-hydroxydeoxyguanosine attenuates doxorubicin-induced cardiotoxicity by decreasing pyroptosis in H9c2 cardiomyocytes.BMC molecular and cell biology · 2022Article
- Article
- BNIP-2 Activation of Cellular Contractility Inactivates YAP for H9c2 Cardiomyoblast Differentiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2022Article
- Innovative Application of Metabolomics on Bioactive Ingredients of Foods.Foods (Basel, Switzerland) · 2022Review
- Protective Effect of Nebivolol against Oxidative Stress Induced by Aristolochic Acids in Endothelial Cells.Toxins · 2022Article
- Untargeted Metabolomics Studies of H9c2 Cardiac Cells Submitted to Oxidative Stress, β-Adrenergic Stimulation and Doxorubicin Treatment: Investigation of Cardiac Biomarkers.Frontiers in molecular biosciences · 2022Article
- Mitochondrial targeted antioxidants, mitoquinone and SKQ1, not vitamin C, mitigate doxorubicin-induced damage in H9c2 myoblast: pretreatment vs. co-treatment.BMC pharmacology & toxicology · 2021Article
- Targeting Metabolic Reprogramming to Improve Breast Cancer Treatment: An In Vitro Evaluation of Selected Metabolic Inhibitors Using a Metabolomic Approach.Metabolites · 2021Article
- Chlorogenic Acid Enhances Doxorubicin-Mediated Cytotoxic Effect in Osteosarcoma Cells.International journal of molecular sciences · 2021Article
- Roflumilast Attenuates Doxorubicin-Induced Cardiotoxicity by Targeting Inflammation and Cellular Senescence in Cardiomyocytes Mediated by SIRT1.Drug design, development and therapy · 2021Article
- NMR as a "Gold Standard" Method in Drug Design and Discovery.Molecules (Basel, Switzerland) · 2020Review
- Article
- A Comparative Study of Rat UrineBiology · 2020Article
- The Prophylactic Effect of Pinocembrin Against Doxorubicin-Induced Cardiotoxicity in anFrontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin (DOX) is an anticancer drug widely used in oncology. The main limitation to DOX treatments though is due to the cumulative dose that may lead to cardiotoxicity. Clinically, DOX-induced cardiomyopathy develops as a progressive heart failure consecutive to a progressive loss in cardiomyocytes due to cell necrosis and apoptosis induced by DOX. For many years, the cardiac oxidative stress caused by DOX was considered as its main toxic mechanism. Therefore, several clinical trials were carried out to assess the efficacy of various antioxidants as a cardioprotective strategy. Only dexrazoxane (DEX), did significantly reduce DOX cardiotoxicity. However, since other antioxidants used later on to counteract DOX cardiotoxicity were not as successful as DEX, DOX-induced oxidative stress and DEX antioxidant activity are not considered as the main feature anymore and this led the scientific world to suspect other involved mechanisms which are still unknown. The objective of the present work was to study from a metabolic point of view the side effects of DOX and the protective properties of DEX.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.