The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling
- Autores
- Vasti, Cecilia; Hertig, Cecilia
- Año de publicación
- 2014
- Idioma
- inglés
- Tipo de recurso
- reseña artículo
- Estado
- versión publicada
- Descripción
- Neuregulin-1 (NRG1) signaling through tyrosine kinase receptors erbB2 and erbB4 was revealed essential for cardiac development as mouse mutated in the Nrg1 or either cognate receptors Erbb2 or Erbb4 genes lack the formation of trabeculae at the ventricular wall. Indeed, the injection of the NRG1 active peptide in developing embryos induced trabeculation of the ventricular free wall. The components of the NRG1 pathway have been identified and the cardiac activities are being progressively characterized. An acquired form of dilated cardiomyopathy was evidenced in a subpopulation of breast tumor patients undergoing a combined treatment with antibodies against erbB2 and chemotherapy. In this regard, the cardiomyocyte-specific gene deletion of either erbb2 or erbb4 leads to ventricular dilation in adult mice, providing an experimental model system to examine the NRG1-mediated activities. We reviewed the evidence on the growing field of research for NRG1 signaling in both cardiac morphogenesis and in the postnatal myocardial remodeling.
Sociedad Argentina de Fisiología - Materia
-
Biología
Neuregulin-1
Remodeling
erbB
Cardiac morphogenesis - Nivel de accesibilidad
- acceso abierto
- Condiciones de uso
- http://creativecommons.org/licenses/by/4.0/
- Repositorio
- Institución
- Universidad Nacional de La Plata
- OAI Identificador
- oai:sedici.unlp.edu.ar:10915/125631
Ver los metadatos del registro completo
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The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodelingVasti, CeciliaHertig, CeciliaBiologíaNeuregulin-1RemodelingerbBCardiac morphogenesisNeuregulin-1 (NRG1) signaling through tyrosine kinase receptors erbB2 and erbB4 was revealed essential for cardiac development as mouse mutated in the Nrg1 or either cognate receptors Erbb2 or Erbb4 genes lack the formation of trabeculae at the ventricular wall. Indeed, the injection of the NRG1 active peptide in developing embryos induced trabeculation of the ventricular free wall. The components of the NRG1 pathway have been identified and the cardiac activities are being progressively characterized. An acquired form of dilated cardiomyopathy was evidenced in a subpopulation of breast tumor patients undergoing a combined treatment with antibodies against erbB2 and chemotherapy. In this regard, the cardiomyocyte-specific gene deletion of either erbb2 or erbb4 leads to ventricular dilation in adult mice, providing an experimental model system to examine the NRG1-mediated activities. We reviewed the evidence on the growing field of research for NRG1 signaling in both cardiac morphogenesis and in the postnatal myocardial remodeling.Sociedad Argentina de Fisiología2014-02info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdf1-13http://sedici.unlp.edu.ar/handle/10915/125631enginfo:eu-repo/semantics/altIdentifier/url/https://pmr.safisiol.org.ar/archive/id/61info:eu-repo/semantics/altIdentifier/issn/1669-5410info:eu-repo/semantics/altIdentifier/issn/1669-5402info:eu-repo/semantics/openAccesshttp://creativecommons.org/licenses/by/4.0/Creative Commons Attribution 4.0 International (CC BY 4.0)reponame:SEDICI (UNLP)instname:Universidad Nacional de La Platainstacron:UNLP2025-09-29T11:30:13Zoai:sedici.unlp.edu.ar:10915/125631Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:30:13.317SEDICI (UNLP) - Universidad Nacional de La Platafalse |
dc.title.none.fl_str_mv |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
title |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
spellingShingle |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling Vasti, Cecilia Biología Neuregulin-1 Remodeling erbB Cardiac morphogenesis |
title_short |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
title_full |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
title_fullStr |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
title_full_unstemmed |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
title_sort |
The role of the neuregulin-1/erbb signaling pathway in cardiac morphogenesis and remodeling |
dc.creator.none.fl_str_mv |
Vasti, Cecilia Hertig, Cecilia |
author |
Vasti, Cecilia |
author_facet |
Vasti, Cecilia Hertig, Cecilia |
author_role |
author |
author2 |
Hertig, Cecilia |
author2_role |
author |
dc.subject.none.fl_str_mv |
Biología Neuregulin-1 Remodeling erbB Cardiac morphogenesis |
topic |
Biología Neuregulin-1 Remodeling erbB Cardiac morphogenesis |
dc.description.none.fl_txt_mv |
Neuregulin-1 (NRG1) signaling through tyrosine kinase receptors erbB2 and erbB4 was revealed essential for cardiac development as mouse mutated in the Nrg1 or either cognate receptors Erbb2 or Erbb4 genes lack the formation of trabeculae at the ventricular wall. Indeed, the injection of the NRG1 active peptide in developing embryos induced trabeculation of the ventricular free wall. The components of the NRG1 pathway have been identified and the cardiac activities are being progressively characterized. An acquired form of dilated cardiomyopathy was evidenced in a subpopulation of breast tumor patients undergoing a combined treatment with antibodies against erbB2 and chemotherapy. In this regard, the cardiomyocyte-specific gene deletion of either erbb2 or erbb4 leads to ventricular dilation in adult mice, providing an experimental model system to examine the NRG1-mediated activities. We reviewed the evidence on the growing field of research for NRG1 signaling in both cardiac morphogenesis and in the postnatal myocardial remodeling. Sociedad Argentina de Fisiología |
description |
Neuregulin-1 (NRG1) signaling through tyrosine kinase receptors erbB2 and erbB4 was revealed essential for cardiac development as mouse mutated in the Nrg1 or either cognate receptors Erbb2 or Erbb4 genes lack the formation of trabeculae at the ventricular wall. Indeed, the injection of the NRG1 active peptide in developing embryos induced trabeculation of the ventricular free wall. The components of the NRG1 pathway have been identified and the cardiac activities are being progressively characterized. An acquired form of dilated cardiomyopathy was evidenced in a subpopulation of breast tumor patients undergoing a combined treatment with antibodies against erbB2 and chemotherapy. In this regard, the cardiomyocyte-specific gene deletion of either erbb2 or erbb4 leads to ventricular dilation in adult mice, providing an experimental model system to examine the NRG1-mediated activities. We reviewed the evidence on the growing field of research for NRG1 signaling in both cardiac morphogenesis and in the postnatal myocardial remodeling. |
publishDate |
2014 |
dc.date.none.fl_str_mv |
2014-02 |
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 |
format |
review |
status_str |
publishedVersion |
dc.identifier.none.fl_str_mv |
http://sedici.unlp.edu.ar/handle/10915/125631 |
url |
http://sedici.unlp.edu.ar/handle/10915/125631 |
dc.language.none.fl_str_mv |
eng |
language |
eng |
dc.relation.none.fl_str_mv |
info:eu-repo/semantics/altIdentifier/url/https://pmr.safisiol.org.ar/archive/id/61 info:eu-repo/semantics/altIdentifier/issn/1669-5410 info:eu-repo/semantics/altIdentifier/issn/1669-5402 |
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info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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openAccess |
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http://creativecommons.org/licenses/by/4.0/ Creative Commons Attribution 4.0 International (CC BY 4.0) |
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application/pdf 1-13 |
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SEDICI (UNLP) - Universidad Nacional de La Plata |
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