ArticleCirculation. Heart failure2025
Heterogeneous Dysregulation of Myosin Super-Relaxation and Energetics in Hypertrophic Cardiomyopathy.
Article in Circulation. Heart failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
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Who cites it
8 citing papers in PubMed.
- Mechanistic diversity within RLC-dependent myosin ATPase inhibitors differentiates EDG-7500, a diastolic-selective cardiac sarcomere modulator.JCI insight · 2026Article
- Immature and mature myocardium in the pathophysiology of hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2026Review
- Load-Dependent Effects of Sodium Glucose Co-Transporter Inhibitors on Work in Human Hypertrophic Cardiomyopathy Living Myocardial Slices.bioRxiv : the preprint server for biology · 2026Article
- A primer on the methods of skeletal and cardiac muscle mechanics using permeabilized preparations.The Journal of general physiology · 2026Review
- Muscle Diffraction at the Life Science X-ray Scattering Beamline.bioRxiv : the preprint server for biology · 2026Article
- Destabilization of cardiac myosin acetylation and sequestration with type 2 diabetes mellitus.Cardiovascular diabetology · 2026Article
- Mavacamten in the Treatment of Obstructive Hypertrophic Cardiomyopathy: from Pathophysiology To Real World Data.Current cardiology reports · 2025Review
- Myosin Mayhem: Losing (or Gaining) Its Chill in Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2025Article
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14 authors.
Funding
Abstract
backgroundHypertrophic cardiomyopathy is often linked to likely pathogenic and pathogenic variants in genes encoding myofilament proteins. The exact molecular mechanisms by which these lead to cardiac dysfunction and metabolic remodeling remain incompletely understood. Hence, here, we sought to determine whether likely pathogenic and pathogenic variants in thick (
methodsWe isolated cardiac strips from the septum of 13 patients with hypertrophic cardiomyopathy with
resultsWe observed that, despite preserved myofilament lattice, likely pathogenic and pathogenic variants in thick and thin filament proteins have opposite effects on cardiac myosin autoinhibition and the subsequent proportion of myosin molecules in the ATP-preserving super-relaxed state. As expected,
conclusionsOur findings indicate that, in hypertrophic cardiomyopathy, cardiac myosin super-relaxed state, associated ATP consumption, and in vitro mavacamten responsiveness depend on the type of myofilament variants. Our data warrant careful analyses of variant-specific responses to myosin inhibitors in the clinic.
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