ReviewPflugers Archiv : European journal of physiology2019
Altered force generation and cell-to-cell contractile imbalance in hypertrophic cardiomyopathy.
Review in Pflugers Archiv : European journal of physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Human iPSC-cardiomyocyte-aggregate cell therapy in non-human primates and correlation of heart recovery with contractile and electrophysiological cardiomyocyte properties.Nature communications · 2026Article
- Early Cytoskeletal Remodeling Drives Hypertrophic Cardiomyopathy Pathogenesis inJournal of cardiovascular development and disease · 2025Article
- A multi-scale finite element method for investigating fiber remodeling in hypertrophic cardiomyopathy.Scientific reports · 2025Article
- A case report of MYH7 mutation-induced restrictive cardiomyopathy.European heart journal. Case reports · 2025Article
- Sarcomeric gene variants among Indians with hypertrophic cardiomyopathy: A scoping review.The Indian journal of medical research · 2023Article
- [Recent research on childhood hypertrophic cardiomyopathy caused byZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Critical Evaluation of Current Hypotheses for the Pathogenesis of Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Review
- AQUA Mutant Protein Quantification of Endomyocardial Biopsy-Sized Samples From a Patient With Hypertrophic Cardiomyopathy.Frontiers in cardiovascular medicine · 2022Article
- Myofibre Hyper-Contractility in Horses Expressing the Myosin Heavy Chain Myopathy Mutation,Cells · 2021Article
- Natural variant frequencies across domains from different sarcomere proteins cross-correlate to identify inter-protein contacts associated with cardiac muscle function and disease.Molecular biomedicine · 2021Article
- Assessment of the Contribution of a Thermodynamic and Mechanical Destabilization of Myosin-Binding Protein C Domain C2 to the Pathomechanism of Hypertrophic Cardiomyopathy-Causing Double MutationInternational journal of molecular sciences · 2021Article
- Myocardial Deformation Analysis inGenes · 2021Article
- Shared Molecular Mechanisms of Hypertrophic Cardiomyopathy and Its Clinical Presentations: Automated Molecular Mechanisms Extraction Approach.Life (Basel, Switzerland) · 2021Article
- Why make a strong muscle weaker?The Journal of general physiology · 2021Article
- Genetic Restrictive Cardiomyopathy: Causes and Consequences-An Integrative Approach.International journal of molecular sciences · 2021Review
- Stochastic allelic expression as trigger for contractile imbalance in hypertrophic cardiomyopathy.Biophysical reviews · 2020Review
- Advanced Evolution of Pathogenesis Concepts in Cardiomyopathies.Journal of clinical medicine · 2019Review
- Electrocardiographic and genetic characteristics in first degree relatives of hypertrophic cardiomyopathy probands: A descriptive cross-sectional study from Vietnam.JRSM cardiovascular diseaseArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM) is mainly caused by mutations in sarcomeric proteins. Thirty to forty percent of identified mutations are found in the ventricular myosin heavy chain (β-MyHC). A common mechanism explaining how numerous mutations in several different proteins induce a similar HCM-phenotype is unclear. It was proposed that HCM-mutations cause hypercontractility, which for some mutations is thought to result from mutation-induced unlocking of myosin heads from a so-called super-relaxed state (SRX). The SRX was suggested to be related to the "interacting head motif," i.e., pairs of myosin heads folded back onto their S2-region. Here, we address these structural states of myosin in context of earlier work on weak binding cross-bridges. However, not all HCM-mutations cause hypercontractility and/or are involved in the interacting head motif. But most likely, all mutations alter the force generating mechanism, yet in different ways, possibly including inhibition of SRX. Such functional-hyper- and hypocontractile-changes are the basis of our previously proposed concept stating that contractile imbalance due to unequal fractions of mutated and wildtype protein among individual cardiomyocytes over time will induce cardiomyocyte disarray and fibrosis, hallmarks of HCM. Studying β-MyHC-mutations, we found substantial contractile variability from cardiomyocyte to cardiomyocyte within a patient's myocardium, much higher than in controls. This was paralleled by a similarly variable fraction of mutant MYH7-mRNA (cell-to-cell allelic imbalance), due to random, burst-like transcription, independent for mutant and wildtype MYH7-alleles. Evidence suggests that HCM-mutations in other sarcomeric proteins follow the same disease mechanism.
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