Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)

Autores
De Giusti, Verónica Celeste; Caldiz, Claudia Irma; Ennis, Irene Lucía; Pérez, Néstor Gustavo; Cingolani, Horacio Eugenio; Aiello, Ernesto Alejandro
Año de publicación
2013
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
Mitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoKATP) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
Materia
Ciencias Médicas
Cardiac myocyte
Reactive oxygen species
Second messenger systems
Sodium-bicarbonate symporters
Sodium-hydrogen antiporter
Nivel de accesibilidad
acceso abierto
Condiciones de uso
http://creativecommons.org/licenses/by/3.0/
Repositorio
SEDICI (UNLP)
Institución
Universidad Nacional de La Plata
OAI Identificador
oai:sedici.unlp.edu.ar:10915/85467

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network_name_str SEDICI (UNLP)
spelling Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)De Giusti, Verónica CelesteCaldiz, Claudia IrmaEnnis, Irene LucíaPérez, Néstor GustavoCingolani, Horacio EugenioAiello, Ernesto AlejandroCiencias MédicasCardiac myocyteReactive oxygen speciesSecond messenger systemsSodium-bicarbonate symportersSodium-hydrogen antiporterMitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoK<SUB>ATP</SUB>) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.Facultad de Ciencias MédicasCentro de Investigaciones Cardiovasculares2013info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdfhttp://sedici.unlp.edu.ar/handle/10915/85467enginfo:eu-repo/semantics/altIdentifier/issn/1664-042Xinfo:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2013.00126info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/3.0/Creative Commons Attribution 3.0 Unported (CC BY 3.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:16:29Zoai:sedici.unlp.edu.ar:10915/85467Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:16:30.178SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
title Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
spellingShingle Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
De Giusti, Verónica Celeste
Ciencias Médicas
Cardiac myocyte
Reactive oxygen species
Second messenger systems
Sodium-bicarbonate symporters
Sodium-hydrogen antiporter
title_short Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
title_full Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
title_fullStr Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
title_full_unstemmed Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
title_sort Mitochondrial reactive oxygen species (ROS) as signaling molecules of intracellular pathways triggered by the cardiac renin-angiotensin II-aldosterone system (RAAS)
dc.creator.none.fl_str_mv De Giusti, Verónica Celeste
Caldiz, Claudia Irma
Ennis, Irene Lucía
Pérez, Néstor Gustavo
Cingolani, Horacio Eugenio
Aiello, Ernesto Alejandro
author De Giusti, Verónica Celeste
author_facet De Giusti, Verónica Celeste
Caldiz, Claudia Irma
Ennis, Irene Lucía
Pérez, Néstor Gustavo
Cingolani, Horacio Eugenio
Aiello, Ernesto Alejandro
author_role author
author2 Caldiz, Claudia Irma
Ennis, Irene Lucía
Pérez, Néstor Gustavo
Cingolani, Horacio Eugenio
Aiello, Ernesto Alejandro
author2_role author
author
author
author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Cardiac myocyte
Reactive oxygen species
Second messenger systems
Sodium-bicarbonate symporters
Sodium-hydrogen antiporter
topic Ciencias Médicas
Cardiac myocyte
Reactive oxygen species
Second messenger systems
Sodium-bicarbonate symporters
Sodium-hydrogen antiporter
dc.description.none.fl_txt_mv Mitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoK<SUB>ATP</SUB>) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.
Facultad de Ciencias Médicas
Centro de Investigaciones Cardiovasculares
description Mitochondria represent major sources of basal reactive oxygen species (ROS) production of the cardiomyocyte. The role of ROS as signaling molecules that mediate different intracellular pathways has gained increasing interest among physiologists in the last years. In our lab, we have been studying the participation of mitochondrial ROS in the intracellular pathways triggered by the renin-angiotensin II-aldosterone system (RAAS) in the myocardium during the past few years. We have demonstrated that acute activation of cardiac RAAS induces mitochondrial ATP-dependent potassium channel (mitoK<SUB>ATP</SUB>) opening with the consequent enhanced production of mitochondrial ROS. These oxidant molecules, in turn, activate membrane transporters, as sodium/hydrogen exchanger (NHE-1) and sodium/bicarbonate cotransporter (NBC) via the stimulation of the ROS-sensitive MAPK cascade. The stimulation of such effectors leads to an increase in cardiac contractility. In addition, it is feasible to suggest that a sustained enhanced production of mitochondrial ROS induced by chronic cardiac RAAS, and hence, chronic NHE-1 and NBC stimulation, would also result in the development of cardiac hypertrophy.
publishDate 2013
dc.date.none.fl_str_mv 2013
dc.type.none.fl_str_mv info:eu-repo/semantics/review
info:eu-repo/semantics/publishedVersion
Revision
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info:ar-repo/semantics/resenaArticulo
format review
status_str publishedVersion
dc.identifier.none.fl_str_mv http://sedici.unlp.edu.ar/handle/10915/85467
url http://sedici.unlp.edu.ar/handle/10915/85467
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/1664-042X
info:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2013.00126
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by/3.0/
Creative Commons Attribution 3.0 Unported (CC BY 3.0)
eu_rights_str_mv openAccess
rights_invalid_str_mv http://creativecommons.org/licenses/by/3.0/
Creative Commons Attribution 3.0 Unported (CC BY 3.0)
dc.format.none.fl_str_mv application/pdf
dc.source.none.fl_str_mv reponame:SEDICI (UNLP)
instname:Universidad Nacional de La Plata
instacron:UNLP
reponame_str SEDICI (UNLP)
collection SEDICI (UNLP)
instname_str Universidad Nacional de La Plata
instacron_str UNLP
institution UNLP
repository.name.fl_str_mv SEDICI (UNLP) - Universidad Nacional de La Plata
repository.mail.fl_str_mv alira@sedici.unlp.edu.ar
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