ReviewNature reviews. Cardiology2017
Unmasking the molecular link between arrhythmogenic cardiomyopathy and Brugada syndrome.
Review in Nature reviews. Cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed.
- Epigenetic regulation of electromechanical continuity might determine phenotypic heterogeneity in SCN5A mutation carriers in Brugada syndrome.Scientific reports · 2025Article
- SCN5A Cardiomyopathy: from Ion Channel Dysfunction To Clinical Disease.Current cardiology reports · 2025Review
- 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
- Transmembrane Protein 43: Molecular and Pathogenetic Implications in Arrhythmogenic Cardiomyopathy and Various Other Diseases.International journal of molecular sciences · 2025Review
- Upregulation of utrophin improves the phenotype of Duchenne muscular dystrophy hiPSC-derived CMs.Molecular therapy. Nucleic acids · 2024Article
- The Role ofCirculation research · 2024Article
- Understanding Arrhythmogenic Cardiomyopathy: Advances through the Use of Human Pluripotent Stem Cell Models.Genes · 2023Review
- Brugada Syndrome: More than a Monogenic Channelopathy.Biomedicines · 2023Review
- Catalytic antibodies in arrhythmogenic cardiomyopathy patients cleave desmoglein 2 and N-cadherin and impair cardiomyocyte cohesion.Cellular and molecular life sciences : CMLS · 2023Article
- Hypertension Induces Pro-arrhythmic Cardiac Connexome Disorders: Protective Effects of Treatment.Biomolecules · 2023Review
- Structural Heart Alterations in Brugada Syndrome: Is it Really a Channelopathy? A Systematic Review.Journal of clinical medicine · 2022Review
- Cellular and Engineered Organoids for Cardiovascular Models.Circulation research · 2022Review
- Clinical Genetics of Inherited Arrhythmogenic Disease in the Pediatric Population.Biomedicines · 2022Review
- Plasma MicroRNAs as noninvasive diagnostic biomarkers in patients with Brugada syndrome.PloS one · 2022Article
- Prevalence and characteristics of the Brugada electrocardiogram pattern in patients with arrhythmogenic right ventricular cardiomyopathy.Journal of arrhythmia · 2021Article
- iPSC-Cardiomyocyte Models of Brugada Syndrome-Achievements, Challenges and Future Perspectives.International journal of molecular sciences · 2021Review
- Recurrent exercise-induced ventricular tachycardia in a patient with Brugada syndrome.HeartRhythm case reports · 2021Article
- Rare Variants Associated with Arrhythmogenic Cardiomyopathy: Reclassification Five Years Later.Journal of personalized medicine · 2021Article
- Evaluating the Use of Genetics in Brugada Syndrome Risk Stratification.Frontiers in cardiovascular medicine · 2021Article
- Brugada Syndrome: Warning of a Systemic Condition?Frontiers in cardiovascular medicine · 2021Review
Corrections and comments
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The intercalated discs that connect cardiomyocytes control cell-to-cell adhesion and communication. Several macromolecular structures (desmosomes, fascia adherens junctions, gap junctions, and sodium-channel complexes) coexist in, and confer their mechanical and electrical properties to, the intercalated disc. Traditionally, each structure was assumed to have a unique function in the intercalated disc. However, growing evidence suggests that these complexes act together in intercellular communication and adhesion, forming a single structural and functional entity - the connexome. This nascent idea has provided conceptual support for the overlapping of two diseases based on disturbance of the intercalated disc - arrhythmogenic cardiomyopathy (ACM) and Brugada syndrome (BrS). In this Perspectives article, we present the latest findings about the functions of, and interactions between, the structures of the intercalated disc that support the concept of the connexome. We also summarize the genetic, molecular, and pathophysiological mechanisms underlying ACM and BrS, focusing on the overlap between these diseases.
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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.