ReviewFrontiers in cardiovascular medicine2022
Thin filament cardiomyopathies: A review of genetics, disease mechanisms, and emerging therapeutics.
Review in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 48 citations in OpenAlex.
- Homozygous TNNC1-A8V Causes Impaired Diastolic Function and Restrictive Cardiomyopathy in Children and Mice.Circulation. Genomic and precision medicine · 2026Article
- A novel missense mutation in tropomyosin 1 gene associated with hypertrophic cardiomyopathy.Journal, genetic engineering & biotechnology · 2026Article
- A homozygous variant in cardiac troponin I3, TNNI3, causes severe pediatric restrictive cardiomyopathy.HGG advances · 2026Article
- Effects of Cardiomyopathic Mutations on the Cytoplasmic Tropomyosin Isoform Tpm1.7.Molecules (Basel, Switzerland) · 2026Article
- Cell-cycle regulation of sarcomere integrity-Role for Actn2 phosphorylation.Physiological reports · 2026Article
- Genetics in Hypertrophic Cardiomyopathy: An Evolving Clinical Landscape.Cardiac failure review · 2026Review
- Multiparametric Assessment of TNNI3 Variant Phenotypes in Human iPSC-Cardiomyocytes Correlates with Disease Severity in Patients.bioRxiv : the preprint server for biology · 2025Article
- LncRNA CISTR-ACT regulates cell size in human and mouse by guiding FOSL2.Nature communications · 2025Article
- TPM2 regulates contractility and biomechanical properties in trabecular meshwork cells.Scientific reports · 2025Article
- Clinical impact of the TPM1 p.Tyr221Cys variant causing hypertrophic cardiomyopathy.Genes & diseases · 2025Article
- Cardiac Troponin C E135A Variant Impairs Myofilament Response to PKA Phosphorylation and Is Associated With Autosomal Dominant Dilated Cardiomyopathy With Diastolic Dysfunction.Circulation. Genomic and precision medicine · 2025Article
- Screening single nucleotide changes to tropomyosin to identify novel cardiomyopathy mutants.Journal of molecular and cellular cardiology · 2025Article
- The L348P point mutation in cardiac myosin binding protein-C alters transient responses to stretch, slows cardiac relaxation, and is embryonic lethal in homozygous CRISPR gene-edited mice.Journal of molecular and cellular cardiology · 2025Article
- Myosin-actin crossbridge independent sarcomere length induced CaJournal of molecular and cellular cardiology · 2025Article
- Review
- Article
- Clinical Features and Prospective Outcomes of Thin-Filament Hypertrophic Cardiomyopathy: Intrinsic Data and Comparative Insights from Other Cohorts.Journal of clinical medicine · 2025Article
- Functional control of myosin motors in the cardiac cycle.Nature reviews. Cardiology · 2025Review
- Troponin I - a comprehensive review of its function, structure, evolution, and role in muscle diseases.Animal cells and systems · 2025Review
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
All muscle contraction occurs due to the cyclical interaction between sarcomeric thin and thick filament proteins within the myocyte. The thin filament consists of the proteins actin, tropomyosin, Troponin C, Troponin I, and Troponin T. Mutations in these proteins can result in various forms of cardiomyopathy, including hypertrophic, restrictive, and dilated phenotypes and account for as many as 30% of all cases of inherited cardiomyopathy. There is significant evidence that thin filament mutations contribute to dysregulation of Ca
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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.