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
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/85467
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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 http://purl.org/coar/resource_type/c_dcae04bc info:ar-repo/semantics/resenaArticulo |
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review |
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publishedVersion |
dc.identifier.none.fl_str_mv |
http://sedici.unlp.edu.ar/handle/10915/85467 |
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http://sedici.unlp.edu.ar/handle/10915/85467 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
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info:eu-repo/semantics/altIdentifier/issn/1664-042X info:eu-repo/semantics/altIdentifier/doi/10.3389/fphys.2013.00126 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/3.0/ Creative Commons Attribution 3.0 Unported (CC BY 3.0) |
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openAccess |
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http://creativecommons.org/licenses/by/3.0/ Creative Commons Attribution 3.0 Unported (CC BY 3.0) |
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