ArticleThe Journal of clinical investigation2015
Bringing home the bacon? The next step in cardiac sodium channelopathies.
Article in The Journal of clinical investigation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 4 citations in OpenAlex.
- Translational Models of Arrhythmia Mechanisms and Susceptibility: Success and Challenges of Modeling Human Disease.Frontiers in cardiovascular medicine · 2019Review
- J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.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 · 2017Review
- J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.Heart rhythm · 2016Review
- J-Wave syndromes expert consensus conference report: Emerging concepts and gaps in knowledge.Journal of arrhythmia · 2016Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in SCN5A, which encodes the α subunit of the major cardiac sodium channel Na(V)1.5, are associated with multiple cardiac arrhythmias, including Brugada syndrome. It is not clear why mutations in SCN5A result in such a variety of cardiac phenotypes, and introduction of analogous Scn5a mutations into small-animal models has not recapitulated alterations in cardiac physiology associated with human disease. In this issue of the JCI, Park and colleagues present a pig model of cardiac sodium channelopathy that was generated by introducing a human Brugada syndrome-associated SCN5A allele. This large-animal model exhibits many phenotypes seen in patients with SCN5A loss-of-function mutations and has the potential to provide important insight into sodium channelopathies.
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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.