Deranged sodium to sudden death

Autores
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; Kaas, Robert S.; Lederer, W. Jonathan; Louch, William E.; Maack, Christoph; Mattiazzi, Ramona Alicia; Qu, Zhilin; Rajamani, Sridharan; Rippinger, Crystal M.; Sejersted, Ole M.; O’Rourke, Brian; Weiss, James N.; Varró, András; Zaza, Antonio
Año de publicación
2015
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
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+ channel structure, function and regulation, and Na+/Ca2+ exchange and Na+/K+ 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+ in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na+-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+ channels and 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.
Fil: Clancy, Colleen E.. University Of California At Davis; Estados Unidos
Fil: Chen Izu, Ye. University Of California At Davis; Estados Unidos
Fil: Bers, Donald M.. University Of California At Davis; Estados Unidos
Fil: Belardinelli, Luiz. Gilead Sciences; Estados Unidos
Fil: Boyden, Penelope A.. Columbia University; Estados Unidos
Fil: Csernoch, Laszlo. University of Debrecen; Hungría
Fil: Despa, Sanda. University Of Kentucky; Estados Unidos
Fil: Fermini, Bernard. Pfizer; Estados Unidos
Fil: Hool, Livia C.. University of Western Australia; Australia
Fil: Izu, Leighton. University Of California At Davis; Estados Unidos
Fil: Kaas, Robert S.. Columbia University; Estados Unidos
Fil: Lederer, W. Jonathan. University of Maryland; Estados Unidos
Fil: Louch, William E.. University Of Oslo; Noruega
Fil: Maack, Christoph. Universitat Saarland; Alemania
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Qu, Zhilin. University of California at Los Angeles; Estados Unidos
Fil: Rajamani, Sridharan. Gilead Sciences; Estados Unidos
Fil: Rippinger, Crystal M.. University Of California At Davis; Estados Unidos
Fil: Sejersted, Ole M.. University Of Oslo; Noruega
Fil: O’Rourke, Brian. University Johns Hopkins; Estados Unidos
Fil: Weiss, James N.. University of California at Los Angeles; Estados Unidos
Fil: Varró, András. University of Szeged; Hungría
Fil: Zaza, Antonio. Universita Degli Studi Di Milano; Italia
Materia
Sodium
Cardiac Disease
Metabolism
Arrhythmias
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/12586

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network_name_str CONICET Digital (CONICET)
spelling Deranged sodium to sudden deathClancy, Colleen E.Chen Izu, YeBers, Donald M.Belardinelli, LuizBoyden, Penelope A.Csernoch, LaszloDespa, SandaFermini, BernardHool, Livia C.Izu, LeightonKaas, Robert S.Lederer, W. JonathanLouch, William E.Maack, ChristophMattiazzi, Ramona AliciaQu, ZhilinRajamani, SridharanRippinger, Crystal M.Sejersted, Ole M.O’Rourke, BrianWeiss, James N.Varró, AndrásZaza, AntonioSodiumCardiac DiseaseMetabolismArrhythmiashttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3In 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+ channel structure, function and regulation, and Na+/Ca2+ exchange and Na+/K+ 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+ in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na+-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+ channels and 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.Fil: Clancy, Colleen E.. University Of California At Davis; Estados UnidosFil: Chen Izu, Ye. University Of California At Davis; Estados UnidosFil: Bers, Donald M.. University Of California At Davis; Estados UnidosFil: Belardinelli, Luiz. Gilead Sciences; Estados UnidosFil: Boyden, Penelope A.. Columbia University; Estados UnidosFil: Csernoch, Laszlo. University of Debrecen; HungríaFil: Despa, Sanda. University Of Kentucky; Estados UnidosFil: Fermini, Bernard. Pfizer; Estados UnidosFil: Hool, Livia C.. University of Western Australia; AustraliaFil: Izu, Leighton. University Of California At Davis; Estados UnidosFil: Kaas, Robert S.. Columbia University; Estados UnidosFil: Lederer, W. Jonathan. University of Maryland; Estados UnidosFil: Louch, William E.. University Of Oslo; NoruegaFil: Maack, Christoph. Universitat Saarland; AlemaniaFil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; ArgentinaFil: Qu, Zhilin. University of California at Los Angeles; Estados UnidosFil: Rajamani, Sridharan. Gilead Sciences; Estados UnidosFil: Rippinger, Crystal M.. University Of California At Davis; Estados UnidosFil: Sejersted, Ole M.. University Of Oslo; NoruegaFil: O’Rourke, Brian. University Johns Hopkins; Estados UnidosFil: Weiss, James N.. University of California at Los Angeles; Estados UnidosFil: Varró, András. University of Szeged; HungríaFil: Zaza, Antonio. Universita Degli Studi Di Milano; ItaliaThe Physiological Society2015-03-15info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/12586Clancy, Colleen E.; Chen Izu, Ye; Bers, Donald M.; Belardinelli, Luiz; Boyden, Penelope A.; et al.; Deranged sodium to sudden death; The Physiological Society; The Journal Of Physiology; 593; 6; 15-3-2015; 1331-13451469-7793enginfo:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2014.281204info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2014.281204/abstractinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T10:18:19Zoai:ri.conicet.gov.ar:11336/12586instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 10:18:19.571CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Deranged sodium to sudden death
title Deranged sodium to sudden death
spellingShingle Deranged sodium to sudden death
Clancy, Colleen E.
Sodium
Cardiac Disease
Metabolism
Arrhythmias
title_short Deranged sodium to sudden death
title_full Deranged sodium to sudden death
title_fullStr Deranged sodium to sudden death
title_full_unstemmed Deranged sodium to sudden death
title_sort Deranged sodium to sudden death
dc.creator.none.fl_str_mv 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
Kaas, Robert S.
Lederer, W. Jonathan
Louch, William E.
Maack, Christoph
Mattiazzi, Ramona Alicia
Qu, Zhilin
Rajamani, Sridharan
Rippinger, Crystal M.
Sejersted, Ole M.
O’Rourke, Brian
Weiss, James N.
Varró, András
Zaza, Antonio
author Clancy, Colleen E.
author_facet 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
Kaas, Robert S.
Lederer, W. Jonathan
Louch, William E.
Maack, Christoph
Mattiazzi, Ramona Alicia
Qu, Zhilin
Rajamani, Sridharan
Rippinger, Crystal M.
Sejersted, Ole M.
O’Rourke, Brian
Weiss, James N.
Varró, András
Zaza, Antonio
author_role author
author2 Chen Izu, Ye
Bers, Donald M.
Belardinelli, Luiz
Boyden, Penelope A.
Csernoch, Laszlo
Despa, Sanda
Fermini, Bernard
Hool, Livia C.
Izu, Leighton
Kaas, Robert S.
Lederer, W. Jonathan
Louch, William E.
Maack, Christoph
Mattiazzi, Ramona Alicia
Qu, Zhilin
Rajamani, Sridharan
Rippinger, Crystal M.
Sejersted, Ole M.
O’Rourke, Brian
Weiss, James N.
Varró, András
Zaza, Antonio
author2_role author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
author
dc.subject.none.fl_str_mv Sodium
Cardiac Disease
Metabolism
Arrhythmias
topic Sodium
Cardiac Disease
Metabolism
Arrhythmias
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv 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+ channel structure, function and regulation, and Na+/Ca2+ exchange and Na+/K+ 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+ in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na+-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+ channels and 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.
Fil: Clancy, Colleen E.. University Of California At Davis; Estados Unidos
Fil: Chen Izu, Ye. University Of California At Davis; Estados Unidos
Fil: Bers, Donald M.. University Of California At Davis; Estados Unidos
Fil: Belardinelli, Luiz. Gilead Sciences; Estados Unidos
Fil: Boyden, Penelope A.. Columbia University; Estados Unidos
Fil: Csernoch, Laszlo. University of Debrecen; Hungría
Fil: Despa, Sanda. University Of Kentucky; Estados Unidos
Fil: Fermini, Bernard. Pfizer; Estados Unidos
Fil: Hool, Livia C.. University of Western Australia; Australia
Fil: Izu, Leighton. University Of California At Davis; Estados Unidos
Fil: Kaas, Robert S.. Columbia University; Estados Unidos
Fil: Lederer, W. Jonathan. University of Maryland; Estados Unidos
Fil: Louch, William E.. University Of Oslo; Noruega
Fil: Maack, Christoph. Universitat Saarland; Alemania
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Cientificas y Tecnicas. Centro Cientifico Tecnológico la Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina. Universidad Nacional de la Plata. Facultad de Ciencias Médicas; Argentina
Fil: Qu, Zhilin. University of California at Los Angeles; Estados Unidos
Fil: Rajamani, Sridharan. Gilead Sciences; Estados Unidos
Fil: Rippinger, Crystal M.. University Of California At Davis; Estados Unidos
Fil: Sejersted, Ole M.. University Of Oslo; Noruega
Fil: O’Rourke, Brian. University Johns Hopkins; Estados Unidos
Fil: Weiss, James N.. University of California at Los Angeles; Estados Unidos
Fil: Varró, András. University of Szeged; Hungría
Fil: Zaza, Antonio. Universita Degli Studi Di Milano; Italia
description 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+ channel structure, function and regulation, and Na+/Ca2+ exchange and Na+/K+ 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+ in the 2014 symposium stemmed from the multitude of recent studies that point to the importance of maintaining Na+ homeostasis in the heart, as disruption of homeostatic processes are increasingly identified in cardiac disease states. Understanding how disruption in cardiac Na+-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+ channels and 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.
publishDate 2015
dc.date.none.fl_str_mv 2015-03-15
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/12586
Clancy, Colleen E.; Chen Izu, Ye; Bers, Donald M.; Belardinelli, Luiz; Boyden, Penelope A.; et al.; Deranged sodium to sudden death; The Physiological Society; The Journal Of Physiology; 593; 6; 15-3-2015; 1331-1345
1469-7793
url http://hdl.handle.net/11336/12586
identifier_str_mv Clancy, Colleen E.; Chen Izu, Ye; Bers, Donald M.; Belardinelli, Luiz; Boyden, Penelope A.; et al.; Deranged sodium to sudden death; The Physiological Society; The Journal Of Physiology; 593; 6; 15-3-2015; 1331-1345
1469-7793
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/doi/10.1113/jphysiol.2014.281204
info:eu-repo/semantics/altIdentifier/url/http://onlinelibrary.wiley.com/doi/10.1113/jphysiol.2014.281204/abstract
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv The Physiological Society
publisher.none.fl_str_mv The Physiological Society
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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