Deranged sodium to sudden death

CLANCY CE; CHEN-IZU Y; BERS DM; BELARDINELLI L; BOYDEN PA; CSERNOCH L; DESPA S; FERMINI B; HOOL LC; IZU L; KASS RS; LEDERER WJ; LOUCH WE; MAACK C; MATTIAZZI AR; QU Z; RAJAMANI S; RIPPINGER CM; SEJERSTED OM; O´ROURKE B; WEISS JN; VARRÓ A; ZAZA A

THE JOURNAL OF PHYSIOLOGY

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2015 vol. 593 p. 1331 - 1345

0022-3751

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 anddiscussion fromthe symposium, with a focuson the role of aberrant sodium channels and abnormal sodium homeostasis in cardiac arrhythmiasand pharmacotherapy from the subcellular scale to the whole heart. Two following papers focuson Na+channel structure, function and regulation, and Na+/Ca2+ exchange and NaATPase.The UC Davis Cardiovascular Symposium is a biannual event that aims to bring together leadingexperts in subfields of cardiovascular biomedicine to focus on topics of importance to the field.The focus on Na+ in the 2014 symposium stemmedfromthe multitude of recent studies that pointto the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostaticprocesses are increasingly identified in cardiac disease states. Understanding how disruptionin cardiac Na+-based processes leads to derangement in multiple cardiac components at thelevel of the cell and to then connect these perturbations to emergent behaviour in the heart tocause disease is a critical area of research. The ubiquity of disruption of Na+ 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