ReviewFrontiers in physiology2019
Mitochondrial Dysfunction as Substrate for Arrhythmogenic Cardiomyopathy: A Search for New Disease Mechanisms.
Review in Frontiers in physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
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Who cites it
24 citing papers in PubMed, 43 citations in OpenAlex.
- Decreasing Microtubule Detyrosination Improves Cardiac Mechanics and Sodium Channel Function in Arrhythmogenic Cardiomyopathy.Circulation. Arrhythmia and electrophysiology · 2026Article
- Disease models and AAV therapies ofMolecular therapy. Advances · 2026Review
- Review
- The mechanism and clinical research of vagus nerve electrical stimulation in the treatment of myocardial ischemia-reperfusion injury.iScience · 2026Review
- Alteplase and Angioedema: Can Clinical Exome Sequencing Redefine the Paradigm?Life (Basel, Switzerland) · 2026Article
- Transcriptomic and proteomic profiling shows dysregulated immune and metabolic pathways in arrhythmogenic cardiomyopathy.ESC heart failure · 2025Article
- CDR1as modulates arrhythmia post-myocardial infarction via regulating Cav1.2.Acta biochimica et biophysica Sinica · 2025Article
- Stellate Ganglia: A Key Therapeutic Target for Malignant Ventricular Arrhythmia in Heart Disease.Circulation research · 2025Review
- Article
- Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy.Biomedicines · 2024Article
- Critical contribution of mitochondria in the development of cardiomyopathy linked to desmin mutation.Stem cell research & therapy · 2024Article
- Omics Analyses of Stromal Cells from ACM Patients Reveal Alterations in Chromatin Organization and Mitochondrial Homeostasis.International journal of molecular sciences · 2023Article
- Review
- GCN5 contributes to intracellular lipid accumulation in human primary cardiac stromal cells from patients affected by Arrhythmogenic cardiomyopathy.Journal of cellular and molecular medicine · 2022Article
- Mitochondrial Dysfunction and Acute Fatty Liver of Pregnancy.International journal of molecular sciences · 2022Review
- Role of plakophilin-2 expression on exercise-related progression of arrhythmogenic right ventricular cardiomyopathy: a translational study.European heart journal · 2022Article
- Oxidized LDL-dependent pathway as new pathogenic trigger in arrhythmogenic cardiomyopathy.EMBO molecular medicine · 2021Article
- Review
- Cobalt oxide nanoparticles induce oxidative stress and alter electromechanical function in rat ventricular myocytes.Particle and fibre toxicology · 2021Article
- Interleukin-1β, Oxidative Stress, and Abnormal Calcium Handling Mediate Diabetic Arrhythmic Risk.JACC. Basic to translational science · 2021Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Arrhythmogenic cardiomyopathy (ACM) is a familial heart disease, associated with ventricular arrhythmias, fibrofatty replacement of the myocardial mass and an increased risk of sudden cardiac death (SCD). Malignant ventricular arrhythmias and SCD largely occur in the pre-clinical phase of the disease, before overt structural changes occur. To prevent or interfere with ACM disease progression, more insight in mechanisms related to electrical instability are needed. Currently, numerous studies are focused on the link between cardiac arrhythmias and metabolic disease. In line with that, a potential role of mitochondrial dysfunction in ACM pathology is unclear and mitochondrial biology in the ACM heart remains understudied. In this review, we explore mitochondrial dysfunction in relation to arrhythmogenesis, and postulate a link to typical hallmarks of ACM. Mitochondrial dysfunction depletes adenosine triphosphate (ATP) production and increases levels of reactive oxygen species in the heart. Both metabolic changes affect cardiac ion channel gating, electrical conduction, intracellular calcium handling, and fibrosis formation; all well-known aspects of ACM pathophysiology. ATP-mediated structural remodeling, apoptosis, and mitochondria-related alterations have already been shown in models of PKP2 dysfunction. Yet, the limited amount of experimental evidence in ACM models makes it difficult to determine whether mitochondrial dysfunction indeed precedes and/or accompanies ACM pathogenesis. Nevertheless, current experimental ACM models can be very useful in unraveling ACM-related mitochondrial biology and in testing potential therapeutic interventions.
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