ArticleFrontiers in pharmacology2020
Imatinib and Dasatinib Provoke Mitochondrial Dysfunction Leading to Oxidative Stress in C2C12 Myotubes and Human RD Cells.
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 24 papers.
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Who cites it
24 citing papers in PubMed, 42 citations in OpenAlex.
- Whole-Genome and Transcriptome Sequencing Identified NOTCH2 and HES1 as Potential Markers of Response to Imatinib in Desmoid Tumor (Aggressive Fibromatosis): A Phase II Trial Study.Cancer research and treatment · 2022Trial
- Enhanced anti-tumor effects of Imatinib and immune checkpoint inhibitors on gastrointestinal stromal tumor cells (GISTs): insights from monoculture and 3D co-culture models.Medical oncology (Northwood, London, England) · 2026Article
- Mitochondrial CaJournal of cellular physiology · 2025Review
- Imatinib-Induced Myopathy in a Patient With Gastrointestinal Stromal Tumor: A Case Report.Cureus · 2025Article
- Drug-induced cytotoxicity prediction in muscle cells, an application of the Cell Painting assay.PloS one · 2025Article
- Imatinib therapy of chronic myeloid leukemia significantly reduces carnitine cell intake, resulting in adverse events.Molecular metabolism · 2024Article
- Inhibition of p53-MDM2 binding reduces senescent cell abundance and improves the adaptive responses of skeletal muscle from aged mice.GeroScience · 2024Article
- Mitochondrial metabolism: a predictive biomarker of radiotherapy efficacy and toxicity.Journal of cancer research and clinical oncology · 2023Review
- Mitochondrial Dysfunction in Cardiotoxicity Induced by BCR-ABL1 Tyrosine Kinase Inhibitors -Underlying Mechanisms, Detection, Potential Therapies.Cardiovascular toxicology · 2023Review
- Adverse effects of tyrosine kinase inhibitors in cancer therapy: pathophysiology, mechanisms and clinical management.Signal transduction and targeted therapy · 2023Review
- PTEN-AKT pathway attenuates apoptosis and adverse remodeling in ponatinib-induced skeletal muscle toxicity following BMP-7 treatment.Physiological reports · 2023Article
- Article
- Peptides GWN and GW protect kidney cells against Dasatinib induced mitochondrial injury in a SIRT1 dependent manner.Food chemistry. Molecular sciences · 2022Article
- Alterations in cellular metabolisms after Imatinib therapy: a review.Medical oncology (Northwood, London, England) · 2022Review
- Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study.Archives of toxicology · 2022Article
- The Role of ROS as a Double-Edged Sword in (In)Fertility: The Impact of Cancer Treatment.Cancers · 2022Review
- Mitochondrial Toxicity Associated with Imatinib and Sorafenib in Isolated Rat Heart Fibers and the Cardiomyoblast H9c2 Cell Line.International journal of molecular sciences · 2022Article
- Alterations in cellular metabolisms after TKI therapy for Philadelphia chromosome-positive leukemia in children: A review.Frontiers in oncology · 2022Review
- Are off-target effects of imatinib the key to improving beta-cell function in diabetes?Upsala journal of medical sciences · 2022Review
- β-Dystroglycan Restoration and Pathology Progression in the DystrophicBiomolecules · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tyrosine kinase inhibitors (TKIs) can cause skeletal muscle toxicity in patients, but the underlying mechanisms are mostly unclear. The goal of the current study was to better characterize the role of mitochondria in TKI-associated myotoxicity. We exposed C2C12 murine myoblasts and myotubes as well as human rhabdomyosarcoma cells (RD cells) for 24 h to imatinib (1-100 µM), erlotinib (1-20 µM), and dasatinib (0.001-100 µM). In C2C12 myoblasts, imatinib was membrane toxic at 50 µM and depleted the cellular ATP pool at 20 µM. In C2C12 myotubes exposed to imatinib, ATP depletion started at 50 µM whereas membrane toxicity was not detectable. In myoblasts and myotubes exposed to dasatinib, membrane toxicity started at 0.5 µM and 2 µM, respectively, and the ATP drop was visible at 0.1 µM and 0.2 µM, respectively. When RD cells were exposed to imatinib, ATP depletion started at 20 µM whereas membrane toxicity was not detectable. Dasatinib was membrane toxic at 20 µM and depleted the cellular ATP pool already at 0.5 µM. Erlotinib was not toxic in both cell models. Imatinib (20 µM) and dasatinib (1 µM) reduced complex I activity in both cell models. Moreover, the mitochondrial membrane potential (
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