ArticlePloS one2016
Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 43 citations in OpenAlex.
- Evaluating the use of rodents as in vitro, in vivo and ex vivo experimental models for the assessment of tyrosine kinase inhibitor-induced cardiotoxicity: a systematic review.Archives of toxicology · 2025Pooled it
- Investigating the Anticancer Effects of Sulforaphane in an In Vitro Coculture Model of Prostate Cancer Cells with Engineered Heart Tissue.ACS pharmacology & translational science · 2025Article
- Novel insights into cardiovascular toxicity of cancer targeted and immune therapies: Beyond ischemia with non-obstructive coronary arteries (INOCA).American heart journal plus : cardiology research and practice · 2024Article
- Vascularised cardiac spheroids-on-a-chip for testing the toxicity of therapeutics.Scientific reports · 2024Article
- Reproducibility of drug-induced effects on the contractility of an engineered heart tissue derived from human pluripotent stem cells.Frontiers in pharmacology · 2023Article
- Predicting individual-specific cardiotoxicity responses induced by tyrosine kinase inhibitors.Frontiers in pharmacology · 2023Article
- Mitochondrial Toxicity Associated with Imatinib and Sorafenib in Isolated Rat Heart Fibers and the Cardiomyoblast H9c2 Cell Line.International journal of molecular sciences · 2022Article
- Building Multi-Dimensional Induced Pluripotent Stem Cells-Based Model Platforms to Assess Cardiotoxicity in Cancer Therapies.Frontiers in pharmacology · 2021Review
- Sodium-Glucose CoTransporter-2 Inhibitor Empagliflozin Ameliorates Sunitinib-Induced Cardiac Dysfunction via Regulation of AMPK-mTOR Signaling Pathway-Mediated Autophagy.Frontiers in pharmacology · 2021Article
- Insulin Resistance and Pellino-1 Mediated Decrease in the Activities of Vasodilator Signaling Contributes to Sunitinib-Induced Hypertension.Frontiers in pharmacology · 2021Article
- Adverse cardiac effects of cancer therapies: cardiotoxicity and arrhythmia.Nature reviews. Cardiology · 2020Review
- Blinded, Multicenter Evaluation of Drug-induced Changes in Contractility Using Human-induced Pluripotent Stem Cell-derived Cardiomyocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Mechanobiology Assays with Applications in Cardiomyocyte Biology and Cardiotoxicity.Advanced healthcare materials · 2020Review
- Tyrosine Kinase Inhibitors in Leukemia and Cardiovascular Events: From Mechanism to Patient Care.Arteriosclerosis, thrombosis, and vascular biology · 2020Review
- A Comprehensive Review of Clinical Cardiotoxicity Incidence of FDA-Approved Small-Molecule Kinase Inhibitors.Frontiers in pharmacology · 2020Review
- Trimetazidine ameliorates sunitinib-induced cardiotoxicity in mice via the AMPK/mTOR/autophagy pathway.Pharmaceutical biology · 2019Article
- Considerations for anFrontiers in pharmacology · 2019Review
- In Silico Pharmacoepidemiologic Evaluation of Drug-Induced Cardiovascular Complications Using Combined Classifiers.Journal of chemical information and modeling · 2018Article
- Exaggerated Cardiotoxicity of Sunitinib in Stressed 3-Dimensional Heart Muscles.JACC. Basic to translational science · 2018Article
- Correction: Analysis of Tyrosine Kinase Inhibitor-Mediated Decline in Contractile Force in Rat Engineered Heart Tissue.PloS one · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 5 institutions in 3 countries.
Funding
Abstract
introductionLeft ventricular dysfunction is a frequent and potentially severe side effect of many tyrosine kinase inhibitors (TKI). The mode of toxicity is not identified, but may include impairment of mitochondrial or sarcomeric function, autophagy or angiogenesis, either as an on-target or off-target mechanism. METHODS AND
resultsWe studied concentration-response curves and time courses for nine TKIs in three-dimensional, force generating engineered heart tissue (EHT) from neonatal rat heart cells. We detected a concentration- and time-dependent decline in contractile force for gefitinib, lapatinib, sunitinib, imatinib, sorafenib, vandetanib and lestaurtinib and no decline in contractile force for erlotinib and dasatinib after 96 hours of incubation. The decline in contractile force was associated with an impairment of autophagy (LC3 Western blot) and appearance of autophagolysosomes (transmission electron microscopy).
conclusionThis study demonstrates the feasibility to study TKI-mediated force effects in EHTs and identifies an association between a decline in contractility and inhibition of autophagic flux.
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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.