ArticleJCI insight2022
Neonatal Scn1b-null mice have sinoatrial node dysfunction, altered atrial structure, and atrial fibrillation.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- SCN5AInternational journal of legal medicine · 2026Article
- Article
- Heterozygous Loss of Scn1b Results in Concealed Conduction Phenotype Unmasked by Osmotic Stress.bioRxiv : the preprint server for biology · 2026Article
- A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure.Nature cardiovascular research · 2026Article
- Unraveling SUDEP: Mechanisms of Seizure-Induced Cardiac and Respiratory Impairment.Epilepsy currents · 2026Article
- Ataxia and cerebellar hypoexcitability in a mouse model of SCN1B-linked Dravet syndrome.JCI insight · 2025Article
- Altered cardiac excitability and arrhythmia in models of SCN1B-linked developmental and epileptic encephalopathy.JCI insight · 2025Article
- Atrial Cardiomyopathy in Atrial Fibrillation: A Multimodal Diagnostic Framework.Diagnostics (Basel, Switzerland) · 2025Review
- Behavioral Abnormalities, Cognitive Impairments, Synaptic Deficits, and Gene Replacement Therapy in a CRISPR Engineered Rat Model of 5p15.2 Deletion Associated With Cri du Chat Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- New focus on cardiac voltage-gated sodium channel β1 and β1B: Novel targets for treating and understanding arrhythmias?Heart rhythm · 2025Review
- Decreased ability to manage increases in reactive oxygen species may underlie susceptibility to arrhythmias in mice lackingAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Atrial cardiomyopathy revisited-evolution of a concept: a clinical consensus statement of the European Heart Rhythm Association (EHRA) of the ESC, the Heart Rhythm Society (HRS), the Asian Pacific Heart Rhythm Society (APHRS), and the Latin American Heart Rhythm Society (LAHRS).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 · 2024Article
- Cardiac sodium channel complexes and arrhythmia: structural and functional roles of the β1 and β3 subunits.The Journal of physiology · 2023Article
- Epilepsy and sudden unexpected death in epilepsy in a mouse model of humanBrain communications · 2023Article
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Authors and funding
14 authors at 2 institutions in 1 country.
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Abstract
Loss-of-function (LOF) variants in SCN1B, encoding the voltage-gated sodium channel β1/β1B subunits, are linked to neurological and cardiovascular diseases. Scn1b-null mice have spontaneous seizures and ventricular arrhythmias and die by approximately 21 days after birth. β1/β1B Subunits play critical roles in regulating the excitability of ventricular cardiomyocytes and maintaining ventricular rhythmicity. However, whether they also regulate atrial excitability is unknown. We used neonatal Scn1b-null mice to model the effects of SCN1B LOF on atrial physiology in pediatric patients. Scn1b deletion resulted in altered expression of genes associated with atrial dysfunction. Scn1b-null hearts had a significant accumulation of atrial collagen, increased susceptibility to pacing induced atrial fibrillation (AF), sinoatrial node (SAN) dysfunction, and increased numbers of cholinergic neurons in ganglia that innervate the SAN. Atropine reduced the incidence of AF in null animals. Action potential duration was prolonged in null atrial myocytes, with increased late sodium current density and reduced L-type calcium current density. Scn1b LOF results in altered atrial structure and AF, demonstrating the critical role played by Scn1b in atrial physiology during early postnatal mouse development. Our results suggest that SCN1B LOF variants may significantly impact the developing pediatric heart.
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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.