ArticleThe Journal of clinical investigation2006
Arrhythmogenic right ventricular cardiomyopathy: moving toward mechanism.
Article in The Journal of clinical investigation, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed.
- Cardiac phenotypes in LMNA mutations.Current opinion in cardiology · 2025Review
- Wnt signaling pathways in biology and disease: mechanisms and therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Current insights into LMNA cardiomyopathies: Existing models and missing LINCs.Nucleus (Austin, Tex.) · 2017Review
- Accelerated cardiac remodeling in desmoplakin transgenic mice in response to endurance exercise is associated with perturbed Wnt/β-catenin signaling.American journal of physiology. Heart and circulatory physiology · 2016Article
- Desmosomes: regulators of cellular signaling and adhesion in epidermal health and disease.Cold Spring Harbor perspectives in medicine · 2014Review
- Plakophilin-2 promotes tumor development by enhancing ligand-dependent and -independent epidermal growth factor receptor dimerization and activation.Molecular and cellular biology · 2014Article
- Structure, function, and regulation of desmosomes.Progress in molecular biology and translational science · 2013Review
- Arrhythmogenic right ventricular cardiomyopathy: an update on pathophysiology, genetics, diagnosis, and risk stratification.Herzschrittmachertherapie & Elektrophysiologie · 2012Review
- Mutations with pathogenic potential in proteins located in or at the composite junctions of the intercalated disk connecting mammalian cardiomyocytes: a reference thesaurus for arrhythmogenic cardiomyopathies and for Naxos and Carvajal diseases.Cell and tissue research · 2012Review
- Plakophilin-2: a cell-cell adhesion plaque molecule of selective and fundamental importance in cardiac functions and tumor cell growth.Cell and tissue research · 2012Article
- Gene Mutations Resulting in the Development of ARVC/D Could Affect Cells of the Cardiac Conduction System.Frontiers in physiology · 2012Article
- Hypertrophic cardiomyopathy.Heart failure clinics · 2010Review
- Interplay of cadherin-mediated cell adhesion and canonical Wnt signaling.Cold Spring Harbor perspectives in biology · 2010Review
- Abnormal connexin43 in arrhythmogenic right ventricular cardiomyopathy caused by plakophilin-2 mutations.Journal of cellular and molecular medicine · 2009Article
- Transcriptional remodeling of rapidly stimulated HL-1 atrial myocytes exhibits concordance with human atrial fibrillation.Journal of molecular and cellular cardiology · 2009Article
- Disparate effects of different mutations in plakoglobin on cell mechanical behavior.Cell motility and the cytoskeleton · 2008Article
- Arrhythmogenic right ventricular cardiomyopathy type 5 is a fully penetrant, lethal arrhythmic disorder caused by a missense mutation in the TMEM43 gene.American journal of human genetics · 2008Article
- Animal models of arrhythmogenic cardiomyopathy.Disease models & mechanismsReview
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in genes encoding desmosomal proteins have been identified as the major cause of arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVC), in which the right ventricle is "replaced" by fibrofatty tissue, resulting in lethal arrhythmias. In this issue of the JCI, Garcia-Gras et al. demonstrate that cardiac-specific loss of the desmosomal protein desmoplakin is sufficient to cause nuclear translocation of plakoglobin, upregulation of adipogenic genes in vitro, and a shift from a cardiomyocyte to an adipocyte cell fate in vivo (see the related article beginning on page 2012). This evidence for potential Wnt/beta-catenin signaling defects sets the scene for a comprehensive exploration of the contributions of this pathway to the pathophysiology of ARVC, not only through perturbation of cardiac patterning and development, but also through effects on myocardial differentiation and physiology.
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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.