ReviewPflugers Archiv : European journal of physiology2014
MYBPC3 in hypertrophic cardiomyopathy: from mutation identification to RNA-based correction.
Review in Pflugers Archiv : European journal of physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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
22 citing papers in PubMed, 45 citations in OpenAlex.
- Multiple triggering mechanisms of myocardial fibrosis: Comparison and integration in different disease contexts.iScience · 2026Review
- Gene therapy in cardiac and vascular diseases: a review of approaches to treat genetic and common cardiovascular diseases with novel gene-based therapeutics.Cardiovascular research · 2025Review
- Pathogenic genes and clinical prognosis in hypertrophic cardiomyopathy.World journal of cardiology · 2025Review
- Myocardial dysfunction caused by MyBPC3 P459fs mutation in hypertrophic cardiomyopathy: evidence from multi-omics approaches and super-resolution imaging.Frontiers in cardiovascular medicine · 2025Article
- Review
- Cardiac myosin-binding protein C N-terminal interactions with myosin and actin filaments: Opposite effects of phosphorylation and M-domain mutations.Journal of molecular and cellular cardiology · 2024Article
- Identification of Two Homozygous Variants inGenes · 2023Article
- MYBPC3 deficiency in cardiac fibroblasts drives their activation and contributes to fibrosis.Cell death & disease · 2022Article
- Modulation of myosin by cardiac myosin binding protein-C peptides improves cardiac contractility in ex-vivo experimental heart failure models.Scientific reports · 2022Article
- Targeted therapies in genetic dilated and hypertrophic cardiomyopathies: from molecular mechanisms to therapeutic targets. A position paper from the Heart Failure Association (HFA) and the Working Group on Myocardial Function of the European Society of Cardiology (ESC).European journal of heart failure · 2022Article
- Review
- An interesting Mybpc3 heterozygous mutation associated with bicuspid aortic valve.Translational pediatrics · 2020Article
- Biomarkers for Heart Failure Prognosis: Proteins, Genetic Scores and Non-coding RNAs.Frontiers in cardiovascular medicine · 2020Review
- Gene therapy strategies in the treatment of hypertrophic cardiomyopathy.Pflugers Archiv : European journal of physiology · 2019Review
- Genotypic effect of a mutation of the MYBPC3 gene and two phenotypes with different patterns of inheritance.Journal of clinical laboratory analysis · 2018Article
- Activation of Autophagy Ameliorates Cardiomyopathy inCirculation. Heart failure · 2017Article
- Evaluation of MYBPC3 trans-Splicing and Gene Replacement as Therapeutic Options in Human iPSC-Derived Cardiomyocytes.Molecular therapy. Nucleic acids · 2017Article
- Review
- Normal cardiac contraction in mice lacking the proline-alanine rich region and C1 domain of cardiac myosin binding protein C.Journal of molecular and cellular cardiology · 2015Article
- I-1-deficiency negatively impacts survival in a cardiomyopathy mouse model.International journal of cardiology. Heart & vasculature · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in MYBPC3 gene, encoding cardiac myosin-binding protein C (cMyBP-C), frequently cause hypertrophic cardiomyopathy (HCM), which affects 0.2 % of the general population. This myocardial autosomal-dominant disorder is the leading cause of sudden cardiac death particularly in young athletes. The current pharmacological and surgical treatments of HCM focus on symptoms relief, but do not address the cause of the disease. With the development of novel strategies targeting the endogenous mutation, causal HCM therapy is now possible. This review will discuss the current knowledge on HCM from the identification of MYBPC3 gene mutations to potential RNA-based correction.
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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.