Deranged sodium to sudden death. (15th March 2015)

• Record Type: Journal Article
• Authors: Clancy, Colleen E.; Chen‐Izu, Ye; Bers, Donald M.; Belardinelli, Luiz; Boyden, Penelope A.; Csernoch, Laszlo; Despa, Sanda; Fermini, Bernard; Hool, Livia C.; Izu, Leighton; Kass, Robert S.; Lederer, W. Jonathan; Louch, William E.; Maack, Christoph; Matiazzi, Alicia; Qu, Zhilin; Rajamani, Sridharan; Rippinger, Crystal M.; Sejersted, Ole M.; O'Rourke, Brian; Weiss, James N.; Varró, András; Zaza, Antonio
• Is Part Of: Journal of physiology. Volume 593:Number 6(2015:Mar.)
• Page Start: 1331
• Page End: 1345
• Publication Date: 2015-03-15
• Subjects: Physiology -- Periodicals; 612.005
• DOI: 10.1113/jphysiol.2014.281204
• Languages: English
• ISSNs: 0022-3751

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="tjp6405-sec-0010" sec-type="section"> <title>Abstract</title> <p>In February 2014, a group of scientists convened as part of the University of California Davis Cardiovascular Symposium to bring together experimental and mathematical modelling perspectives and discuss points of consensus and controversy on the topic of sodium in the heart. This paper summarizes the topics of presentation and discussion from the symposium, with a focus on the role of aberrant sodium channels and abnormal sodium homeostasis in cardiac arrhythmias and pharmacotherapy from the subcellular scale to the whole heart. Two following papers focus on Na<sup>+</sup> channel structure, function and regulation, and Na<sup>+</sup>/Ca<sup>2+</sup> exchange and Na<sup>+</sup>/K<sup>+</sup> ATPase. The UC Davis Cardiovascular Symposium is a biannual event that aims to bring together leading experts in subfields of cardiovascular biomedicine to focus on topics of importance to the field. The focus on Na<sup>+</sup> in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na<sup>+</sup> homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na<sup>+</sup>‐based processes leads to derangement in multiple cardiac components at the level of the cell and to then connect these perturbations to emergent behaviour in the heart to cause disease is a critical area of research. The ubiquity of disruption of Na<sup>+</sup> channels and Na<sup>+</sup> homeostasis in cardiac disorders of excitability and mechanics emphasizes the importance of a fundamental understanding of the associated mechanisms and disease processes to ultimately reveal new targets for human therapy.</p> </sec> </abstract>