ArticleToxicology2015
Identification of novel biomarkers for doxorubicin-induced toxicity in human cardiomyocytes derived from pluripotent stem cells.
Article in Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 82 citations in OpenAlex.
- Revisiting Secondary Dilative Cardiomyopathy.International journal of molecular sciences · 2025Pooled it
- Progressive suppression of DNA repair genes with persistent p53 target activation in doxorubicin-treated cardiomyocytes.G3 (Bethesda, Md.) · 2026Article
- SWATH-MS for discovery of early biomarkers of drug-induced cardiotoxicity using an animal doxorubicin model.Cardio-oncology (London, England) · 2026Article
- Article
- Gold(III) Complexes with Aromatic Cyano-Substituted Bisdithiolate Ligands as Potential Anticancer and Antimicrobial Agents.Molecules (Basel, Switzerland) · 2025Article
- MO Oxygen Therapy Prevents Doxorubicin-Induced Cardiotoxicity.Cardiology research and practice · 2025Article
- Applications, Limitations, and Considerations of Clinical Trials in a Dish.Bioengineering (Basel, Switzerland) · 2024Review
- Recent advances in pluripotent stem cell-derived cardiac organoids and heart-on-chip applications for studying anti-cancer drug-induced cardiotoxicity.Cell biology and toxicology · 2023Review
- Molecular basis of GDF15 induction and suppression by drugs in cardiomyocytes and cancer cells toward precision medicine.Scientific reports · 2023Article
- Review
- Circulating biomarkers for management of cancer therapeutics-related cardiac dysfunction.Cardiovascular research · 2023Review
- In vitro to clinical translational pharmacokinetic/pharmacodynamic modeling of doxorubicin (DOX) and dexrazoxane (DEX) interactions: Safety assessment and optimization.Scientific reports · 2023Article
- Predicting individual-specific cardiotoxicity responses induced by tyrosine kinase inhibitors.Frontiers in pharmacology · 2023Article
- microRNAs signatures as potential biomarkers of structural cardiotoxicity in human-induced pluripotent stem-cell derived cardiomyocytes.Archives of toxicology · 2022Article
- Preclinical In Vitro Model to Assess the Changes in Permeability and Cytotoxicity of Polarized Intestinal Epithelial Cells during Exposure Mimicking Oral or Intravenous Routes: An Example of Arsenite Exposure.International journal of molecular sciences · 2022Article
- Chronic Cardiotoxicity Assays Using Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes (hiPSC-CMs).International journal of molecular sciences · 2022Review
- Unravelling Mechanisms of Doxorubicin-Induced Toxicity in 3D Human Intestinal Organoids.International journal of molecular sciences · 2022Article
- Article
- CRISPR/Cas9-mediated generation and analysis of N terminus polymorphic models of βMolecular therapy. Methods & clinical development · 2021Article
- The mRNA expression ofMolecular medicine reports · 2021Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Doxorubicin is a chemotherapeutic agent indicated for the treatment of a variety of cancer types, including leukaemia, lymphomas, and many solid tumours. The use of doxorubicin is, however, associated with severe cardiotoxicity, often resulting in early discontinuation of the treatment. Importantly, the toxic symptoms can occur several years after the termination of the doxorubicin administration. In this study, the toxic effects of doxorubicin exposure have been investigated in cardiomyocytes derived from human embryonic stem cells (hESC). The cells were exposed to different concentrations of doxorubicin for up to 2 days, followed by a 12 day recovery period. Notably, the cell morphology was altered during drug treatment and the cells showed a reduced contractile ability, most prominent at the highest concentration of doxorubicin at the later time points. A general cytotoxic response measured as Lactate dehydrogenase leakage was observed after 2 days' exposure compared to the vehicle control, but this response was absent during the recovery period. A similar dose-dependant pattern was observed for the release of cardiac specific troponin T (cTnT) after 1 day and 2 days of treatment with doxorubicin. Global transcriptional profiles in the cells revealed clusters of genes that were differentially expressed during doxorubicin exposure, a pattern that in some cases was sustained even throughout the recovery period, suggesting that these genes could be used as sensitive biomarkers for doxorubicin-induced toxicity in human cardiomyocytes. The results from this study show that cTnT release can be used as a measurement of acute cardiotoxicity due to doxorubicin. However, for the late onset of doxorubicin-induced cardiomyopathy, cTnT release might not be the most optimal biomarker. As an alternative, some of the genes that we identified as differentially expressed after doxorubicin exposure could serve as more relevant biomarkers, and may also help to explain the cellular mechanisms behind the late onset apoptosis associated with doxorubicin-induced cardiomyopathy.
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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 OpenQuestion graph.