Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis

Autores
Mattiazzi, Alicia Ramona; Vittone, Leticia; Mundiña-Weilenmann, Cecilia
Año de publicación
2007
Idioma
inglés
Tipo de recurso
reseña artículo
Estado
versión publicada
Descripción
Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.
Facultad de Ciencias Médicas
Materia
Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
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:10915/83199
Acceder
id SEDICI_81a578f28f25d5bfff61a6684d9854fe
oai_identifier_str oai:sedici.unlp.edu.ar:10915/83199
network_acronym_str SEDICI
repository_id_str 1329
network_name_str SEDICI (UNLP)
spelling Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosisMattiazzi, Alicia RamonaVittone, LeticiaMundiña-Weilenmann, CeciliaCiencias MédicasAcidosisCaMKIIProtein phosphorylationSR functionIntracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.Facultad de Ciencias Médicas2007info:eu-repo/semantics/reviewinfo:eu-repo/semantics/publishedVersionRevisionhttp://purl.org/coar/resource_type/c_dcae04bcinfo:ar-repo/semantics/resenaArticuloapplication/pdf648-656http://sedici.unlp.edu.ar/handle/10915/83199enginfo:eu-repo/semantics/altIdentifier/issn/0008-6363info:eu-repo/semantics/altIdentifier/doi/10.1016/j.cardiores.2006.12.002info: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:UNLP2025-09-29T11:15:41Zoai:sedici.unlp.edu.ar:10915/83199Institucionalhttp://sedici.unlp.edu.ar/Universidad públicaNo correspondehttp://sedici.unlp.edu.ar/oai/snrdalira@sedici.unlp.edu.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:13292025-09-29 11:15:42.224SEDICI (UNLP) - Universidad Nacional de La Platafalse
dc.title.none.fl_str_mv Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
spellingShingle Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
Mattiazzi, Alicia Ramona
Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
title_short Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_full Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_fullStr Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_full_unstemmed Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
title_sort Ca2+/calmodulin-dependent protein kinase: A key component in the contractile recovery from acidosis
dc.creator.none.fl_str_mv Mattiazzi, Alicia Ramona
Vittone, Leticia
Mundiña-Weilenmann, Cecilia
author Mattiazzi, Alicia Ramona
author_facet Mattiazzi, Alicia Ramona
Vittone, Leticia
Mundiña-Weilenmann, Cecilia
author_role author
author2 Vittone, Leticia
Mundiña-Weilenmann, Cecilia
author2_role author
author
dc.subject.none.fl_str_mv Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
topic Ciencias Médicas
Acidosis
CaMKII
Protein phosphorylation
SR function
dc.description.none.fl_txt_mv Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.
Facultad de Ciencias Médicas
description Intracellular acidosis exerts substantial effects on the contractile performance of the heart. Soon after the onset of acidosis, contractility diminishes, largely due to a decrease in myofilament Ca2+ responsiveness. This decrease in contractility is followed by a progressive recovery that occurs despite the persistent acidosis. This recovery is the result of different mechanisms that converge to increase diastolic Ca2+ levels and Ca2+ transient amplitude. Recent experimental evidence indicates that activation of the Ca2+/calmodulin-dependent protein kinase II (CaMKII) is an essential step in the sequence of events that increases the Ca2+ transient amplitude and produces contractile recovery. CaMKII may act as an amplifier, providing compensatory pathways to offset the inhibitory effects of acidosis on many of the Ca2+ handling proteins. CaMKII-induced phosphorylation of the SERCA2a regulatory protein phospholamban (PLN) has the potential to promote an increase in sarcoplasmic reticulum (SR) Ca2+ uptake and SR Ca2+ load, and is a likely candidate to mediate the mechanical recovery from acidosis. In addition, CaMKII-dependent phosphorylation of proteins other than PLN may also contribute to this recovery.
publishDate 2007
dc.date.none.fl_str_mv 2007
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/10915/83199
url http://sedici.unlp.edu.ar/handle/10915/83199
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/issn/0008-6363
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.cardiores.2006.12.002
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)
dc.format.none.fl_str_mv application/pdf
648-656
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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score 13.070432

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