ReviewCirculation research2011
Thin filament mutations: developing an integrative approach to a complex disorder.
Review in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 118 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.
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Who cites it
118 citing papers in PubMed, 150 citations in OpenAlex.
- Mutation specific impairment of fatty acid and pyruvate oxidation in hypertrophic cardiomyopathy mouse models.Journal of molecular and cellular cardiology · 2026Article
- Redox Imbalance and Genetic Mutations in Heart Failure: Synergistic Mechanisms and Therapeutic Strategies.Genes · 2026Review
- The Structural Role of Tropomyosin in Regulating Thin Filament Activation of Actin-Myosin Interaction.Sub-cellular biochemistry · 2026Review
- Relationship between genotype and clinical phenotype of hypertrophic cardiomyopathy.World journal of cardiology · 2025Review
- Resolving the structure and dynamics of the disordered C terminus of human cardiac troponin T and effects of cardiomyopathic mutations.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Velcro-binding by cardiac troponin-I traps tropomyosin on actin in a low-energy relaxed state.Biochemical and biophysical research communications · 2025Article
- The transmission of mutation effects in a multiprotein machine: A comprehensive metadynamics study of the cardiac thin filament.Protein science : a publication of the Protein Society · 2024Article
- Natural history and clinical outcomes of patients with hypertrophic cardiomyopathy from thin filament mutations.ESC heart failure · 2024Review
- Dilated Cardiomyopathy - Exploring the Underlying Causes.Medical research archives · 2024Article
- Allele-specific dysregulation of lipid and energy metabolism in early-stage hypertrophic cardiomyopathy.Journal of molecular and cellular cardiology plus · 2024Article
- Myosin's powerstroke transitions define atomic scale movement of cardiac thin filament tropomyosin.The Journal of general physiology · 2024Article
- Mechanism-based myofilament manipulation to treat diastolic dysfunction in HFpEF.Frontiers in physiology · 2024Review
- Novel Mutation Glu98Lys in Cardiac Tropomyosin Alters Its Structure and Impairs Myocardial Relaxation.International journal of molecular sciences · 2023Article
- Thin filament regulation of cardiac muscle power output: Implications for targets to improve human failing hearts.The Journal of general physiology · 2023Article
- De Novo Asp219Val Mutation in Cardiac Tropomyosin Associated with Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2022Article
- The effect of MgThe FEBS journal · 2022Article
- Restrictive cardiomyopathy: definition and diagnosis.European heart journal · 2022Article
- Low expression of the K280NJournal of molecular and cellular cardiology plus · 2022Article
- Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics.International journal of molecular sciences · 2022Review
- Hypertrophic cardiomyopathy: Mutations to mechanisms to therapies.Frontiers in physiology · 2022Review
58 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Sixteen years ago, mutations in cardiac troponin (Tn)T and α-tropomyosin were linked to familial hypertrophic cardiomyopathy, thus transforming the disorder from a disease of the β-myosin heavy chain to a disease of the cardiac sarcomere. From the outset, studies suggested that mutations in the regulatory thin filament caused a complex, heterogeneous pattern of ventricular remodeling with wide variations in clinical expression. To date, the clinical heterogeneity is well matched by an extensive array of nearly 100 independent mutations in all components of the cardiac thin filament. Significant advances in our understanding of the biophysics of myofilament activation, coupled to the emerging evidence that thin filament linked cardiomyopathies are progressive, suggests that a renewed focus on the most proximal events in both the molecular and clinical pathogenesis of the disease will be necessary to achieve the central goal of using genotype information to manage affected patients. In this review, we examine the existing biophysical and clinical evidence in support of a more proximal definition of thin filament cardiomyopathies. In addition, new high-resolution, integrated approaches are presented to help define the way forward as the field works toward developing a more robust link between genotype and phenotype in this complex disorder.
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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.