ArticleJournal of molecular medicine (Berlin, Germany)2009
Decreased contractility due to energy deprivation in a transgenic rat model of hypertrophic cardiomyopathy.
Article in Journal of molecular medicine (Berlin, Germany), 2009. 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, 42 citations in OpenAlex.
- A multi-scale finite element method for investigating fiber remodeling in hypertrophic cardiomyopathy.Scientific reports · 2025Article
- Adenosine triphosphate-induced cell death in heart failure: Is there a link?World journal of cardiology · 2025Review
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Molecular and metabolic landscape of adenosine triphosphate-induced cell death in cardiovascular disease.World journal of cardiology · 2024Review
- Mechano-energetic efficiency in patients with hypertrophic cardiomyopathy with and without sarcomeric mutations.Journal of cardiovascular translational research · 2024Article
- Mechanisms and prognostic impact of myocardial ischaemia in hypertrophic cardiomyopathy.The international journal of cardiovascular imaging · 2023Review
- Slower Calcium Handling Balances Faster Cross-Bridge Cycling in HumanCirculation research · 2023Article
- The relation between sarcomere energetics and the rate of isometric tension relaxation in healthy and diseased cardiac muscle.Journal of muscle research and cell motility · 2021Article
- Proteomic and Functional Studies Reveal Detyrosinated Tubulin as Treatment Target in Sarcomere Mutation-Induced Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2021Article
- Activation of Cannabinoid Receptors Attenuates Endothelin-1-Induced Mitochondrial Dysfunction in Rat Ventricular Myocytes.Journal of cardiovascular pharmacology · 2020Article
- The homozygous K280N troponin T mutation alters cross-bridge kinetics and energetics in human HCM.The Journal of general physiology · 2019Article
- Mitochondrial Dysfunctions Contribute to Hypertrophic Cardiomyopathy in Patient iPSC-Derived Cardiomyocytes with MT-RNR2 Mutation.Stem cell reports · 2018Article
- The novel cardiac z-disc protein CEFIP regulates cardiomyocyte hypertrophy by modulating calcineurin signaling.The Journal of biological chemistry · 2017Article
- Delineation of Molecular Pathways Involved in Cardiomyopathies Caused by Troponin T Mutations.Molecular & cellular proteomics : MCP · 2016Article
- Myoscape controls cardiac calcium cycling and contractility via regulation of L-type calcium channel surface expression.Nature communications · 2016Article
- Mechanotransduction and Metabolism in Cardiomyocyte Microdomains.BioMed research international · 2016Review
- Muscle dysfunction in hypertrophic cardiomyopathy: what is needed to move to translation?Journal of muscle research and cell motility · 2014Review
- Hypothesis and theory: mechanical instabilities and non-uniformities in hereditary sarcomere myopathies.Frontiers in physiology · 2014Article
- Mechanisms of disease: hypertrophic cardiomyopathy.Nature reviews. Cardiology · 2011Review
- Increased myofilament Ca2+-sensitivity and arrhythmia susceptibility.Journal of molecular and cellular cardiology · 2010Review
Corrections and comments
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Authors and funding
15 authors at 7 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is associated with cardiac hypertrophy, diastolic dysfunction, and sudden death. Recently, it has been suggested that inefficient energy utilization could be a common molecular pathway of HCM-related mutations. We have previously generated transgenic Sprague-Dawley rats overexpressing a truncated cardiac troponin T (DEL-TNT) molecule, displaying typical features of HCM such as diastolic dysfunction and an increased susceptibility to ventricular arrhythmias. We now studied these rats using 31P magnetic resonance spectroscopy (MRS). MRS demonstrated that cardiac energy metabolism was markedly impaired, as indicated by a decreased phosphocreatine to ATP ratio (-31%, p < 0.05). In addition, we assessed contractility of isolated cardiomyocytes. While DEL-TNT and control cardiomyocytes showed no difference under baseline conditions, DEL-TNT cardiomyocytes selectively exhibited a decrease in fractional shortening by 28% after 1 h in glucose-deprived medium (p < 0.05). Moreover, significant decreases in contraction velocity and relaxation velocity were observed. To identify the underlying molecular pathways, we performed transcriptional profiling using real-time PCR. DEL-TNT hearts exhibited induction of several genes critical for cardiac energy supply, including CD36, CPT-1/-2, and PGC-1alpha. Finally, DEL-TNT rats and controls were studied by radiotelemetry after being stressed by isoproterenol, revealing a significantly increased frequency of arrhythmias in transgenic animals. In summary, we demonstrate profound energetic alterations in DEL-TNT hearts, supporting the notion that inefficient cellular ATP utilization contributes to the pathogenesis of HCM.
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