Na+-H+ exchanger inhibition : A new antihypertrophic tool

Autores
Cingolani, Horacio Eugenio; Camilión de Hurtado, María Cristina
Año de publicación
2002
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Cardiac hypertrophy (CH) is a major risk factor for cardiac death and commonly precedes the development of heart failure (HF). This is motivating the search for novel pharmacological strategies to prevent the development and/or regress CH. Although the signaling pathways leading to myocardial hypertrophy are complex, one important set of pathways involves the mitogen-activated protein kinases (MAPKs). MAPKs phosphorylate numerous substrates, including nuclear transcription factors that activate the expression of different genes. The Na+-H+ exchanger (NHE) is a common downstream effector of this cascade and has been implicated in different models of hypertrophy, such as “hypertensive” myocardium, aortic constrictioninduced hypertrophy, and postinfarction myocardial hypertrophy. Interestingly, stretch-induced hypertrophy of cultured neonatal cardiomyocytes is also accompanied by an increase in MAPK activity and NHE activation. Furthermore, stretch-induced MAPK stimulation is partially prevented by inhibition of NHE activity.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Cardiac hypertrophy
Na+-H+ exchanger
NHE1 inhibitors
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by-nc-sa/4.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/84978

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network_name_str SEDICI (UNLP)
spelling Na+-H+ exchanger inhibition : A new antihypertrophic toolCingolani, Horacio EugenioCamilión de Hurtado, María CristinaCiencias MédicasCardiac hypertrophyNa+-H+ exchangerNHE1 inhibitorsCardiac hypertrophy (CH) is a major risk factor for cardiac death and commonly precedes the development of heart failure (HF). This is motivating the search for novel pharmacological strategies to prevent the development and/or regress CH. Although the signaling pathways leading to myocardial hypertrophy are complex, one important set of pathways involves the mitogen-activated protein kinases (MAPKs). MAPKs phosphorylate numerous substrates, including nuclear transcription factors that activate the expression of different genes. The Na<SUP>+</SUP>-H<SUP>+</SUP> exchanger (NHE) is a common downstream effector of this cascade and has been implicated in different models of hypertrophy, such as “hypertensive” myocardium, aortic constrictioninduced hypertrophy, and postinfarction myocardial hypertrophy. Interestingly, stretch-induced hypertrophy of cultured neonatal cardiomyocytes is also accompanied by an increase in MAPK activity and NHE activation. Furthermore, stretch-induced MAPK stimulation is partially prevented by inhibition of NHE activity.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2002info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionArticulohttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdf751-753http://sedici.unlp.edu.ar/handle/10915/84978enginfo:eu-repo/semantics/altIdentifier/issn/0009-7330info:eu-repo/semantics/altIdentifier/doi/10.1161/01.RES.0000016836.24179.AEinfo:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by-nc-sa/4.0/Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2026-02-26T11:03:26Zoai:sedici.unlp.edu.ar:10915/84978Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292026-02-26 11:03:26.495SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Na+-H+ exchanger inhibition : A new antihypertrophic tool
title Na+-H+ exchanger inhibition : A new antihypertrophic tool
spellingShingle Na+-H+ exchanger inhibition : A new antihypertrophic tool
Cingolani, Horacio Eugenio
Ciencias Médicas
Cardiac hypertrophy
Na+-H+ exchanger
NHE1 inhibitors
title_short Na+-H+ exchanger inhibition : A new antihypertrophic tool
title_full Na+-H+ exchanger inhibition : A new antihypertrophic tool
title_fullStr Na+-H+ exchanger inhibition : A new antihypertrophic tool
title_full_unstemmed Na+-H+ exchanger inhibition : A new antihypertrophic tool
title_sort Na+-H+ exchanger inhibition : A new antihypertrophic tool
dc.creator.none.fl_str_mv Cingolani, Horacio Eugenio
Camilión de Hurtado, María Cristina
author Cingolani, Horacio Eugenio
author_facet Cingolani, Horacio Eugenio
Camilión de Hurtado, María Cristina
author_role author
author2 Camilión de Hurtado, María Cristina
author2_role author
dc.subject.none.fl_str_mv Ciencias Médicas
Cardiac hypertrophy
Na+-H+ exchanger
NHE1 inhibitors
topic Ciencias Médicas
Cardiac hypertrophy
Na+-H+ exchanger
NHE1 inhibitors
dc.description.none.fl_txt_mv Cardiac hypertrophy (CH) is a major risk factor for cardiac death and commonly precedes the development of heart failure (HF). This is motivating the search for novel pharmacological strategies to prevent the development and/or regress CH. Although the signaling pathways leading to myocardial hypertrophy are complex, one important set of pathways involves the mitogen-activated protein kinases (MAPKs). MAPKs phosphorylate numerous substrates, including nuclear transcription factors that activate the expression of different genes. The Na<SUP>+</SUP>-H<SUP>+</SUP> exchanger (NHE) is a common downstream effector of this cascade and has been implicated in different models of hypertrophy, such as “hypertensive” myocardium, aortic constrictioninduced hypertrophy, and postinfarction myocardial hypertrophy. Interestingly, stretch-induced hypertrophy of cultured neonatal cardiomyocytes is also accompanied by an increase in MAPK activity and NHE activation. Furthermore, stretch-induced MAPK stimulation is partially prevented by inhibition of NHE activity.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
description Cardiac hypertrophy (CH) is a major risk factor for cardiac death and commonly precedes the development of heart failure (HF). This is motivating the search for novel pharmacological strategies to prevent the development and/or regress CH. Although the signaling pathways leading to myocardial hypertrophy are complex, one important set of pathways involves the mitogen-activated protein kinases (MAPKs). MAPKs phosphorylate numerous substrates, including nuclear transcription factors that activate the expression of different genes. The Na<SUP>+</SUP>-H<SUP>+</SUP> exchanger (NHE) is a common downstream effector of this cascade and has been implicated in different models of hypertrophy, such as “hypertensive” myocardium, aortic constrictioninduced hypertrophy, and postinfarction myocardial hypertrophy. Interestingly, stretch-induced hypertrophy of cultured neonatal cardiomyocytes is also accompanied by an increase in MAPK activity and NHE activation. Furthermore, stretch-induced MAPK stimulation is partially prevented by inhibition of NHE activity.
publishDate 2002
dc.date.none.fl_str_mv 2002
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Articulo
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info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/84978
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dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0009-7330
info:eu-repo/semantics/altIdentifier/doi/10.1161/01.RES.0000016836.24179.AE
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by-nc-sa/4.0/
Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0)
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751-753
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