Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension

Autores
Egan, Benova T.; Szeiffova, Bacova B.; Viczenczova, C; Diez, Emiliano Raúl; Barancik, M.; Tribulova, N.
Año de publicación
2016
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of lifethreatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that downregulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.
Fil: Egan, Benova T.. Institute For Heart Research; Eslovaquia
Fil: Szeiffova, Bacova B.. Institute For Heart Research; Eslovaquia
Fil: Viczenczova, C. Institute For Heart Research,; Eslovaquia
Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Cs.médicas. Cátedra de Fisiología Humana Normal; Argentina
Fil: Barancik, M.. Institute For Heart Research,; Eslovaquia
Fil: Tribulova, N.. Institute For Heart Research,; Eslovaquia
Materia
Hypertension
Arrhythmias
Connexin-43
Cardioprotection
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/49802
Acceder
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repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertensionEgan, Benova T.Szeiffova, Bacova B.Viczenczova, CDiez, Emiliano RaúlBarancik, M.Tribulova, N.HypertensionArrhythmiasConnexin-43Cardioprotectionhttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of lifethreatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that downregulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.Fil: Egan, Benova T.. Institute For Heart Research; EslovaquiaFil: Szeiffova, Bacova B.. Institute For Heart Research; EslovaquiaFil: Viczenczova, C. Institute For Heart Research,; EslovaquiaFil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Cs.médicas. Cátedra de Fisiología Humana Normal; ArgentinaFil: Barancik, M.. Institute For Heart Research,; EslovaquiaFil: Tribulova, N.. Institute For Heart Research,; EslovaquiaAcad Sciences Czech Republic2016-09info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/49802Egan, Benova T.; Szeiffova, Bacova B.; Viczenczova, C; Diez, Emiliano Raúl; Barancik, M.; et al.; Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension; Acad Sciences Czech Republic; Physiological Research; 65; Suppl. 1; 9-2016; 29-420862-8408CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/http://www.biomed.cas.cz/physiolres/pdf/65%20Suppl%201/65_S29.pdfinfo:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T09:55:33Zoai:ri.conicet.gov.ar:11336/49802instacron: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:34982025-09-03 09:55:34.129CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
title Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
spellingShingle Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
Egan, Benova T.
Hypertension
Arrhythmias
Connexin-43
Cardioprotection
title_short Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
title_full Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
title_fullStr Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
title_full_unstemmed Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
title_sort Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension
dc.creator.none.fl_str_mv Egan, Benova T.
Szeiffova, Bacova B.
Viczenczova, C
Diez, Emiliano Raúl
Barancik, M.
Tribulova, N.
author Egan, Benova T.
author_facet Egan, Benova T.
Szeiffova, Bacova B.
Viczenczova, C
Diez, Emiliano Raúl
Barancik, M.
Tribulova, N.
author_role author
author2 Szeiffova, Bacova B.
Viczenczova, C
Diez, Emiliano Raúl
Barancik, M.
Tribulova, N.
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Hypertension
Arrhythmias
Connexin-43
Cardioprotection
topic Hypertension
Arrhythmias
Connexin-43
Cardioprotection
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of lifethreatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that downregulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.
Fil: Egan, Benova T.. Institute For Heart Research; Eslovaquia
Fil: Szeiffova, Bacova B.. Institute For Heart Research; Eslovaquia
Fil: Viczenczova, C. Institute For Heart Research,; Eslovaquia
Fil: Diez, Emiliano Raúl. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Mendoza. Instituto de Medicina y Biología Experimental de Cuyo; Argentina. Universidad Nacional de Cuyo. Facultad de Cs.médicas. Cátedra de Fisiología Humana Normal; Argentina
Fil: Barancik, M.. Institute For Heart Research,; Eslovaquia
Fil: Tribulova, N.. Institute For Heart Research,; Eslovaquia
description Gap junction connexin channels are important determinants of myocardial conduction and synchronization that is crucial for coordinated heart function. One of the main risk factors for cardiovascular events that results in heart attack, congestive heart failure, stroke as well as sudden arrhythmic death is hypertension. Mislocalization and/or dysfunction of specific connexin-43 channels due to hypertension-induced myocardial remodeling have been implicated in the occurrence of lifethreatening arrhythmias and heart failure in both, humans as well as experimental animals. Recent studies suggest that downregulation of myocardial connexin-43, its abnormal distribution and/or phosphorylation might be implicated in this process. On the other hand, treatment of hypertensive animals with cardioprotective drugs (e.g. statins) or supplementation with non-pharmacological compounds, such as melatonin, omega-3 fatty acids and red palm oil protects from lethal arrhythmias. The antiarrhythmic effects are attributed to the attenuation of myocardial connexin-43 abnormalities associated with preservation of myocardial architecture and improvement of cardiac conduction. Findings uncover novel mechanisms of cardioprotective (antihypertensive and antiarrhythmic) effects of compounds that are used in clinical settings. Well-designed trials are needed to explore the antiarrhythmic potential of these compounds in patients suffering from hypertension.
publishDate 2016
dc.date.none.fl_str_mv 2016-09
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/11336/49802
Egan, Benova T.; Szeiffova, Bacova B.; Viczenczova, C; Diez, Emiliano Raúl; Barancik, M.; et al.; Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension; Acad Sciences Czech Republic; Physiological Research; 65; Suppl. 1; 9-2016; 29-42
0862-8408
CONICET Digital
CONICET
url http://hdl.handle.net/11336/49802
identifier_str_mv Egan, Benova T.; Szeiffova, Bacova B.; Viczenczova, C; Diez, Emiliano Raúl; Barancik, M.; et al.; Protection of cardiac cell-to-cell coupling attenuate myocardial remodeling and proarrhythmia induced by hypertension; Acad Sciences Czech Republic; Physiological Research; 65; Suppl. 1; 9-2016; 29-42
0862-8408
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/http://www.biomed.cas.cz/physiolres/pdf/65%20Suppl%201/65_S29.pdf
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Acad Sciences Czech Republic
publisher.none.fl_str_mv Acad Sciences Czech Republic
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
_version_ 1842269352771977216
score 13.13397

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