ReviewInternational journal of molecular sciences2020
Established and Emerging Mechanisms in the Pathogenesis of Arrhythmogenic Cardiomyopathy: A Multifaceted Disease.
Review in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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
20 citing papers in PubMed, 26 citations in OpenAlex.
- Precision Cardiogenomics in Athletes.International journal of molecular sciences · 2026Review
- Review
- Transcriptomic and proteomic profiling shows dysregulated immune and metabolic pathways in arrhythmogenic cardiomyopathy.ESC heart failure · 2025Article
- Molecular Pathogenesis of Arrhythmogenic Cardiomyopathy: Mechanisms and Therapeutic Perspectives.Biomolecules · 2025Review
- Unraveling "Hot Phases" of Arrhythmogenic Cardiomyopathy.JACC. Basic to translational science · 2025Article
- Targeting Canonical Wnt-signaling Through GSK-3β in Arrhythmogenic Cardiomyopathy: Conservative or Progressive?Journal of cardiovascular translational research · 2025Review
- Article
- Article
- Review
- PITX2 induction leads to impaired cardiomyocyte function in arrhythmogenic cardiomyopathy.Stem cell reports · 2023Article
- Using Zebrafish Animal Model to Study the Genetic Underpinning and Mechanism of Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2023Review
- Modeling incomplete penetrance in arrhythmogenic cardiomyopathy by human induced pluripotent stem cell derived cardiomyocytes.Computational and structural biotechnology journal · 2023Article
- The role of β-catenin in cardiac diseases.Frontiers in pharmacology · 2023Review
- Non Coding RNAs as Regulators of Wnt/β-Catenin and Hippo Pathways in Arrhythmogenic Cardiomyopathy.Biomedicines · 2022Review
- Arrhythmogenic Cardiomyopathy: Exercise Pitfalls, Role of Connexin-43, and Moving beyond Antiarrhythmics.International journal of molecular sciences · 2022Review
- Atomic Force Microscopy (AFM) Applications in Arrhythmogenic Cardiomyopathy.International journal of molecular sciences · 2022Review
- Activation of PDGFRA signaling contributes to filamin C-related arrhythmogenic cardiomyopathy.Science advances · 2022Article
- Translation of New and Emerging Therapies for Genetic Cardiomyopathies.JACC. Basic to translational science · 2022Review
- Desmosomes: emerging pathways and non-canonical functions in cardiac arrhythmias and disease.Biophysical reviews · 2021Review
- Editorial of Special Issue "Genetics and Molecular Pathogenesis of Non-Ischemic Cardiomyopathies".International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a heritable myocardial disease that manifests with cardiac arrhythmias, syncope, sudden cardiac death, and heart failure in the advanced stages. The pathological hallmark of ACM is a gradual replacement of the myocardium by fibroadiposis, which typically starts from the epicardium. Molecular genetic studies have identified causal mutations predominantly in genes encoding for desmosomal proteins; however, non-desmosomal causal mutations have also been described, including genes coding for nuclear proteins, cytoskeleton componentsand proteins involved in excitation-contraction coupling. Despite the poor prognosis, currently available treatments can only partially control symptoms and to date there is no effective therapy for ACM. Inhibition of the canonical Wnt/β-catenin pathway and activation of the Hippo and the TGF-β pathways have been implicated in the pathogenesis of ACM. Yet, our understanding of the molecular mechanisms involved in the development of the disease and the cell source of fibroadiposis remains incomplete. Elucidation of the pathogenesis of the disease could facilitate targeted approaches for treatment. In this manuscript we will provide a comprehensive review of the proposed molecular and cellular mechanisms of the pathogenesis of ACM, including the emerging evidence on abnormal calcium homeostasis and inflammatory/autoimmune response. Moreover, we will propose novel hypothesis about the role of epicardial cells and paracrine factors in the development of the phenotype. Finally, we will discuss potential innovative therapeutic approaches based on the growing knowledge in the field.
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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.