ArticleThe Journal of physiology2025
Cardiac sympathetic neurons are additional cells affected in genetically determined arrhythmogenic cardiomyopathy.
Article in The Journal of physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- A reproducible and physiologically relevant human iPSC-derived platform for in vitro modeling of the neurocardiac junction.Molecular therapy : the journal of the American Society of Gene Therapy · 2026Article
- Review
- Advances in autonomic neuromodulation for cardiac arrhythmias: Shifting paradigms in pathophysiology and therapeutics.Heart rhythm · 2026Article
- Acute arrhythmias in a long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency mouse model.American journal of physiology. Heart and circulatory physiology · 2026Article
- Exercise-induced dysregulation of the adrenergic response in a mouse model of PKP2-arrhythmogenic cardiomyopathy.Heart rhythm · 2025Article
- Precision sampling of discrete sites identified during in-vivo functional testing in the mammalian heart.Communications engineering · 2024Article
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Authors and funding
12 authors.
Funding
Abstract
Arrhythmogenic cardiomyopathy (AC) is a familial cardiac disease, mainly caused by mutations in desmosomal genes, which accounts for most cases of stress-related arrhythmic sudden death, in young and athletes. AC hearts display fibro-fatty lesions that generate the arrhythmic substrate and cause contractile dysfunction. A correlation between physical/emotional stresses and arrhythmias supports the involvement of sympathetic neurons (SNs) in the disease, but this has not been confirmed previously. Here, we combined molecular, in vitro and ex vivo analyses to determine the role of AC-linked DSG2 downregulation on SN biology and assess cardiac sympathetic innervation in desmoglein-2 mutant (Dsg2
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