ReviewCell communication & adhesion2014
Remodeling of cell-cell junctions in arrhythmogenic cardiomyopathy.
Review in Cell communication & adhesion, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
17 citing papers in PubMed, 30 citations in OpenAlex.
- Desmoplakin Loss Leads to PKC- and Src-Mediated Contractile Dysfunction in Cardiomyocytes.Circulation research · 2026Article
- Comprehensive analysis of desmosomal protein remodelling identifies desmocollin-2 as potential biomarker for arrhythmogenic cardiomyopathy.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Sex-specific response to A1BG loss results in female dilated cardiomyopathy.Biology of sex differences · 2025Article
- Cardiac sympathetic neurons are additional cells affected in genetically determined arrhythmogenic cardiomyopathy.The Journal of physiology · 2025Article
- Cheek-Pro-Heart: What Can the Buccal Mucosa Do for Arrhythmogenic Cardiomyopathy?Biomedicines · 2023Review
- "Orphan" Connexin43 in Plakophilin-2 Deficient Hearts Revealed by Volume Electron Microscopy.Frontiers in cell and developmental biology · 2022Article
- Plakophilin-2 truncating variants impair cardiac contractility by disrupting sarcomere stability and organization.Science advances · 2021Article
- Genes, other than Muc5b, play a role in bleomycin-induced lung fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- Arrhythmogenic Cardiomyopathy Is a Multicellular Disease Affecting Cardiac and Bone Marrow Mesenchymal Stromal Cells.Journal of clinical medicine · 2021Article
- Disruption of CaCirculation · 2019Article
- Molecular mechanisms of arrhythmogenic cardiomyopathy.Nature reviews. Cardiology · 2019Review
- Reduced desmoplakin immunofluorescence signal in arrhythmogenic cardiomyopathy with epicardial right ventricular outflow tract tachycardia.HeartRhythm case reports · 2019Article
- Desmoplakin maintains gap junctions by inhibiting Ras/MAPK and lysosomal degradation of connexin-43.The Journal of cell biology · 2018Article
- Reversing Mechanoinductive DSP Expression by CRISPR/dCas9-mediated Epigenome Editing.American journal of respiratory and critical care medicine · 2018Article
- Desmoplakin Variants Are Associated with Idiopathic Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2016Article
- GSK3- and PRMT-1-dependent modifications of desmoplakin control desmoplakin-cytoskeleton dynamics.The Journal of cell biology · 2015Article
- Comparative proteomic analysis of human lung telocytes with fibroblasts.Journal of cellular and molecular medicine · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Arrhythmogenic cardiomyopathy (AC) is a primary myocardial disorder characterized by a high incidence of ventricular arrhythmias often preceding the onset of ventricular remodeling and dysfunction. Approximately 50% of patients diagnosed with AC have one or more mutations in genes encoding desmosomal proteins, although non-desmosomal genes have also been associated with the disease. Increasing evidence implicates remodeling of intercalated disk proteins reflecting abnormal responses to mechanical load and aberrant cell signaling pathways in the pathogenesis of AC. This review summarizes recent advances in understanding disease mechanisms in AC that have come from studies of human myocardium and experimental models.
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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.