ArticleToxicology and applied pharmacology2008
Chronic pharmacologic inhibition of EGFR leads to cardiac dysfunction in C57BL/6J mice.
Article in Toxicology and applied pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 35 citations in OpenAlex.
- Major adverse cardiovascular events in advanced-stage lung cancer: a multicenter cohort study.Therapeutic advances in medical oncology · 2024Article
- Decoding of miR-7-5p in Colony Forming Unit-Hill Colonies as a Biomarker of Subclinical Cardiovascular Disease-A MERIT Study.International journal of molecular sciences · 2023Article
- Cardiovascular toxicity of tyrosine kinase inhibitors during cancer treatment: Potential involvement of TRPM7.Frontiers in cardiovascular medicine · 2023Review
- Cardiac pericyte reprogramming by MEK inhibition promotes arteriologenesis and angiogenesis of the ischemic heart.The Journal of clinical investigation · 2022Article
- Epidermal growth factor receptor-dependent maintenance of cardiac contractility.Cardiovascular research · 2022Article
- The Role of Epidermal Growth Factor Receptor Family of Receptor Tyrosine Kinases in Mediating Diabetes-Induced Cardiovascular Complications.Frontiers in pharmacology · 2021Review
- Article
- Cardiac GPCR-Mediated EGFR Transactivation: Impact and Therapeutic Implications.Journal of cardiovascular pharmacology · 2017Review
- Epidermal Growth Factor Receptor Transactivation: Mechanisms, Pathophysiology, and Potential Therapies in the Cardiovascular System.Annual review of pharmacology and toxicology · 2016Article
- Diabetic cardiomyopathy: Role of epidermal growth factor receptor tyrosine kinase.Journal of molecular and cellular cardiology · 2015Article
- Temporal and gefitinib-sensitive regulation of cardiac cytokine expression via chronic β-adrenergic receptor stimulation.American journal of physiology. Heart and circulatory physiology · 2015Article
- Moderate inappropriately high aldosterone/NaCl constellation in mice: cardiovascular effects and the role of cardiovascular epidermal growth factor receptor.Scientific reports · 2014Article
- The role of epidermal growth factor receptor in diabetes-induced cardiac dysfunction.BioImpacts : BI · 2013Article
- The EGFR tyrosine kinase inhibitor tyrphostin AG-1478 causes hypomagnesemia and cardiac dysfunction.Canadian journal of physiology and pharmacology · 2012Article
- The epidermal growth factor receptor is involved in angiotensin II but not aldosterone/salt-induced cardiac remodelling.PloS one · 2012Article
- Article
- Involvement of Depressive Catecholamines as Thrombosis Risk/Inflammatory Markers in Non-Smoker, Non-Obese Congestive Heart Failure, Linked to Increased Epidermal Growth Factor-Receptor (EGF-R) Production.Indian journal of clinical biochemistry : IJCB · 2011Article
- Epidermal growth factor protects the heart against low-flow ischemia-induced injury.Journal of physiology and biochemistry · 2010Article
- Reduced EGFR causes abnormal valvular differentiation leading to calcific aortic stenosis and left ventricular hypertrophy in C57BL/6J but not 129S1/SvImJ mice.American journal of physiology. Heart and circulatory physiology · 2009Article
- The role of Neuregulin-1beta/ErbB signaling in the heart.Experimental cell research · 2009Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Molecule-targeted therapies like those against the epidermal growth factor receptor (EGFR) are becoming widely used in the oncology clinic. With improvements in treatment efficacy, many cancers are being treated as chronic diseases, with patients having prolonged exposure to several therapies that were previously only given acutely. The consequence of chronic suppression of EGFR activity may lead to unexpected toxicities like altered cardiac physiology, a common organ site for adverse drug effects. To explore this possibility, we treated C57BL/6J (B6) mice with two EGFR small molecule tyrosine kinase inhibitors (TKIs), irreversible EKB-569 and reversible AG-1478, orally for 3 months. In B6 female mice, chronic exposure to both TKIs depressed body weight gain and caused significant changes in left ventricular (LV) wall thickness and cardiac function. No significant differences were observed in heart weight or cardiomyocyte size but histological analysis revealed an increase in fibrosis and in the numbers of TUNEL-positive cells in the hearts from treated female mice. Consistent with histological results, LV apoptotic gene expression was altered, with significant downregulation of the anti-apoptotic gene Bcl2l1. Although there were no significant differences in any of these endpoints in treated male mice, suggesting sex may influence susceptibility to TKI mediated toxicity, the LVs of treated male mice had significant upregulation of Egf, Erbb2 and Nppb over controls. Taken together, these data suggest that chronic dietary exposure to TKIs may result in pathological and physiological changes in the heart.
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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.