Altered cardiac energetics in mice lacking Scn1b
Author:
Affiliation:
1. Quillen College of Medicine, Department of Biomedical Sciences, East Tennessee State University , Johnson City, TN 37614 , USA
Funder
National Institute of Neurological Disorders
National Institutes of Health
Research Development Committee at East Tennessee State University
Publisher
Oxford University Press (OUP)
Link
https://academic.oup.com/cardiovascres/advance-article-pdf/doi/10.1093/cvr/cvae087/57287424/cvae087.pdf
Reference14 articles.
1. Sodium channel β subunits: emerging targets in channelopathies;O’Malley;Annu Rev Physiol,2015
2. Voltage-gated sodium channel β1/β1B subunits regulate cardiac physiology and pathophysiology;Edokobi;Front Physiol,2018
3. Sodium channel Scn1b null mice exhibit prolonged QT and RR intervals;Lopez-Santiago;J Mol Cell Cardiol,2007
4. Channelopathy as a SUDEP biomarker in Dravet syndrome patient-derived cardiac myocytes;Frasier;Stem Cell Reports,2018
5. Mitochondrial permeability transition in the diabetic heart: contributions of thiol redox state and mitochondrial calcium to augmented reperfusion injury;Sloan;J Mol Cell Cardiol,2012
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1. Decreased ability to manage increases in reactive oxygen species may underlie susceptibility to arrhythmias in mice lacking Scn1b;American Journal of Physiology-Heart and Circulatory Physiology;2024-10-01
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