ReviewJournal of cardiovascular translational research2009
Mechanical and energetic consequences of HCM-causing mutations.
Review in Journal of cardiovascular translational research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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.
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Who cites it
41 citing papers in PubMed.
- Probing relaxed myosin states in hypertrophic cardiomyopathy by second harmonic-generation microscopy.eLife · 2026Article
- Mitochondrial tRNAHuman mutation · 2026Article
- Imaging of metabolic dysfunction in genetic cardiomyopathies.The international journal of cardiovascular imaging · 2025Review
- Imaging myocardial scar in hypertrophic cardiomyopathy: advances in CMR and CT.Frontiers in cardiovascular medicine · 2025Review
- Myocardial contractility characteristics of hypertrophic cardiomyopathy patients with and without sarcomere mutation.Heart and vessels · 2024Article
- Evolving Strategies for the Management of Obstructive Hypertrophic Cardiomyopathy.Journal of cardiac failure · 2024Review
- Metabolic remodeling and calcium handling abnormality in induced pluripotent stem cell-derived cardiomyocytes in dilated phase of hypertrophic cardiomyopathy with MYBPC3 frameshift mutation.Scientific reports · 2024Article
- FARS2 Deficiency Causes Cardiomyopathy by Disrupting Mitochondrial Homeostasis and the Mitochondrial Quality Control System.Circulation · 2024Article
- Differences in Androgen Receptor Expression in Human Heart Tissue in Various Types of Cardiomyopathy and in Aortic Valve Stenosis.Journal of cardiovascular development and disease · 2023Article
- Slower Calcium Handling Balances Faster Cross-Bridge Cycling in HumanCirculation research · 2023Article
- Mitochondrial ATP Synthase Tetramer Disassembly following Blood-Based or del Nido Cardioplegia during Neonatal Cardiac Surgery.The journal of extra-corporeal technology · 2022Article
- Review
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Prospects for remodeling the hypertrophic heart with myosin modulators.Frontiers in cardiovascular medicine · 2022Review
- Altered Cardiac Energetics and Mitochondrial Dysfunction in Hypertrophic Cardiomyopathy.Circulation · 2021Article
- Article
- Pathophysiology and Treatment of Hypertrophic Cardiomyopathy: New Perspectives.Current heart failure reports · 2021Review
- Mavacamten has a differential impact on force generation in myofibrils from rabbit psoas and human cardiac muscle.The Journal of general physiology · 2021Article
- T-tubule remodeling in human hypertrophic cardiomyopathy.Journal of muscle research and cell motility · 2021Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Hypertrophic cardiomyopathy (HCM) was the first inherited heart disease to be characterized at the molecular genetic level with the demonstration that it is caused by mutations in genes that encode different components of the cardiac sarcomere. Early functional in vitro studies have concluded that HCM mutations cause a loss of sarcomere mechanical function. Hypertrophy would then follow as a compensatory mechanism to raise the work and power output of the affected heart. More recent in vitro and mouse model studies have suggested that HCM mutations enhance contractile function and myofilament Ca(2+) sensitivity and impair cardiac myocyte energetics. It has been hypothesized that these changes may result in cardiac myocyte energy depletion due to inefficient ATP utilization and also in altered myoplasmic Ca(2+) handling. The problems encountered in reaching a definitive answer on the effects of HCM mutations are discussed. Though direct analysis of the altered functional characteristics of HCM human cardiac sarcomeres has so far lagged behind the in vitro and mouse studies, recent work with mechanically isolated skinned myocytes and myofibrils from affected human hearts seem to support the energy depletion hypothesis. If further validated in the human heart, this hypothesis would identify tractable therapeutic targets that suggest that HCM, perhaps more than any other cardiomyopathy, will be amenable to disease-modifying therapy.
Indexed as
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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.