ReviewThe Journal of experimental biology2016
Effects of hypertrophic and dilated cardiomyopathy mutations on power output by human β-cardiac myosin.
Review in The Journal of experimental biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 70 citations in OpenAlex.
- Force-Induced Ankle Opening Reveals Mechanical Stabilization of the Ankle of Human β-Cardiac Myosin.ACS nano · 2026Article
- Hypertrophic cardiomyopathy mutations Y115H and E497D disrupt the folded-back state of human β-cardiac myosin allosterically.Nature communications · 2025Article
- Myocardial contractility characteristics of hypertrophic cardiomyopathy patients with and without sarcomere mutation.Heart and vessels · 2024Article
- Reassessing the unifying hypothesis for hypercontractility caused by myosin mutations in hypertrophic cardiomyopathy.The EMBO journal · 2024Review
- Cardiac troponin I directly binds and inhibits mitochondrial ATP synthase with a noncanonical role in the post-ischemic heart.Nature cardiovascular research · 2024Article
- Toward physics-based precision medicine: Exploiting protein dynamics to design new therapeutics and interpret variants.Protein science : a publication of the Protein Society · 2024Review
- Age and Sex Differences in the Genetics of Cardiomyopathy.Journal of cardiovascular translational research · 2023Article
- Regulated cell death pathways in cardiomyopathy.Acta pharmacologica Sinica · 2023Review
- Cryo-EM structure of the folded-back state of human β-cardiac myosin.Nature communications · 2023Article
- Cryo-EM structure of the folded-back state of human β-cardiac myosin.bioRxiv : the preprint server for biology · 2023Article
- Safety, tolerability, pharmacokinetics, and pharmacodynamics of single and multiple doses of aficamten in healthy Chinese participants: a randomized, double-blind, placebo-controlled, phase 1 study.Frontiers in pharmacology · 2023Article
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Left ventricular outflow tract obstruction in hypertrophic cardiomyopathy and the impact of mavacamten.Therapeutic advances in chronic disease · 2022Review
- Prospects for remodeling the hypertrophic heart with myosin modulators.Frontiers in cardiovascular medicine · 2022Review
- Review
- Cardiac myosin contraction and mechanotransduction in health and disease.The Journal of biological chemistry · 2021Review
- Mavacamten has a differential impact on force generation in myofibrils from rabbit psoas and human cardiac muscle.The Journal of general physiology · 2021Article
- Sarcomere mutation negative hypertrophic cardiomyopathy is associated with ageing and obesity.Open heart · 2021Article
- Small Molecules acting on Myofilaments as Treatments for Heart and Skeletal Muscle Diseases.International journal of molecular sciences · 2020Review
- M8R tropomyosin mutation disrupts actin binding and filament regulation: The beginning affects the middle and end.The Journal of biological chemistry · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Hypertrophic cardiomyopathy is the most frequently occurring inherited cardiovascular disease, with a prevalence of more than one in 500 individuals worldwide. Genetically acquired dilated cardiomyopathy is a related disease that is less prevalent. Both are caused by mutations in the genes encoding the fundamental force-generating protein machinery of the cardiac muscle sarcomere, including human β-cardiac myosin, the motor protein that powers ventricular contraction. Despite numerous studies, most performed with non-human or non-cardiac myosin, there is no clear consensus about the mechanism of action of these mutations on the function of human β-cardiac myosin. We are using a recombinantly expressed human β-cardiac myosin motor domain along with conventional and new methodologies to characterize the forces and velocities of the mutant myosins compared with wild type. Our studies are extending beyond myosin interactions with pure actin filaments to include the interaction of myosin with regulated actin filaments containing tropomyosin and troponin, the roles of regulatory light chain phosphorylation on the functions of the system, and the possible roles of myosin binding protein-C and titin, important regulatory components of both cardiac and skeletal muscles.
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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.