CaMKII: A link between metabolic disorders and cardiac arrhythmias

Autores
Federico, Marilén; Valverde, Carlos Alfredo; Gonano, Luis Alberto; Palomeque, Julieta; Mattiazzi, Ramona Alicia
Año de publicación
2023
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
The prevalence of metabolic diseases -such as obesity, prediabetes, metabolic syndrome or diabetes-has increased globally over the years. These diseases, mainly diabetes mellitus (DM), are among the leading causes of mortality and morbidity worldwide, with increased risk of diabetic cardiomyopathy (DC), cardiac arrhythmias, and heart failure (HF).In metabolic diseases several steps and proteins involved in excitation-contraction coupling (ECC) are compromised, precluding an efficient and rhythmic cardiac contraction; moreover, calcium/calmodulin-dependent protein kinase II (CaMKII) a kinase involved in ECC, is upregulated in several metabolic maladies and significantly contributes to cardiac remodeling and arrhythmias, among which are calcium (Ca2+)-triggered arrhythmias. CaMKII activation is canonically produced by an increase and binding of Ca2+-calmodulin followed by auto-phosphorylation; furthermore, it may occur as a result of several post-translational modifications, including oxidation and O-GlcNAcylation that are usually present in metabolic illnesses and support chronic CaMKII upregulation and ECC impairment.The aim of the present review is to summarize what is known about the different pathways modifying CaMKII activity and Ca2+ handling in metabolic disorders and may promote Ca2+-triggered arrhythmias even at the early stages of metabolic alterations. Future challenges in this field may encompass unraveling the precise mechanisms by which metabolic disturbances modulate CaMKII activity and its downstream effects on cardiac electrophysiology among different species. This would allow the development of robust and valid preclinical human models that can accurately recapitulate the pathophysiology of the human heart. Additionally, investigating the impact of targeted interventions, such as pharmacological inhibitors or gene therapies, could provide valuable insights into the feasibility and efficacy of manipulating CaMKII signaling to prevent or treat arrhythmias in metabolic disorders.
Fil: Federico, Marilén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Palomeque, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Materia
CaMKII
diabetes
metabolic syndrome
heart
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/255843
Acceder
id CONICETDig_aeabc4aa5b00e08d1c56681089f50b8d
oai_identifier_str oai:ri.conicet.gov.ar:11336/255843
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling CaMKII: A link between metabolic disorders and cardiac arrhythmiasFederico, MarilénValverde, Carlos AlfredoGonano, Luis AlbertoPalomeque, JulietaMattiazzi, Ramona AliciaCaMKIIdiabetesmetabolic syndromehearthttps://purl.org/becyt/ford/3.1https://purl.org/becyt/ford/3The prevalence of metabolic diseases -such as obesity, prediabetes, metabolic syndrome or diabetes-has increased globally over the years. These diseases, mainly diabetes mellitus (DM), are among the leading causes of mortality and morbidity worldwide, with increased risk of diabetic cardiomyopathy (DC), cardiac arrhythmias, and heart failure (HF).In metabolic diseases several steps and proteins involved in excitation-contraction coupling (ECC) are compromised, precluding an efficient and rhythmic cardiac contraction; moreover, calcium/calmodulin-dependent protein kinase II (CaMKII) a kinase involved in ECC, is upregulated in several metabolic maladies and significantly contributes to cardiac remodeling and arrhythmias, among which are calcium (Ca2+)-triggered arrhythmias. CaMKII activation is canonically produced by an increase and binding of Ca2+-calmodulin followed by auto-phosphorylation; furthermore, it may occur as a result of several post-translational modifications, including oxidation and O-GlcNAcylation that are usually present in metabolic illnesses and support chronic CaMKII upregulation and ECC impairment.The aim of the present review is to summarize what is known about the different pathways modifying CaMKII activity and Ca2+ handling in metabolic disorders and may promote Ca2+-triggered arrhythmias even at the early stages of metabolic alterations. Future challenges in this field may encompass unraveling the precise mechanisms by which metabolic disturbances modulate CaMKII activity and its downstream effects on cardiac electrophysiology among different species. This would allow the development of robust and valid preclinical human models that can accurately recapitulate the pathophysiology of the human heart. Additionally, investigating the impact of targeted interventions, such as pharmacological inhibitors or gene therapies, could provide valuable insights into the feasibility and efficacy of manipulating CaMKII signaling to prevent or treat arrhythmias in metabolic disorders.Fil: Federico, Marilén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Palomeque, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaFil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; ArgentinaElsevier2023-12info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/255843Federico, Marilén; Valverde, Carlos Alfredo; Gonano, Luis Alberto; Palomeque, Julieta; Mattiazzi, Ramona Alicia; CaMKII: A link between metabolic disorders and cardiac arrhythmias; Elsevier; Aspects of Molecular Medicine; 2; 12-2023; 1-112949-6888CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S2949688823000229info:eu-repo/semantics/altIdentifier/doi/10.1016/j.amolm.2023.100022info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-nd/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-03T10:01:23Zoai:ri.conicet.gov.ar:11336/255843instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-03 10:01:25.166CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv CaMKII: A link between metabolic disorders and cardiac arrhythmias
title CaMKII: A link between metabolic disorders and cardiac arrhythmias
spellingShingle CaMKII: A link between metabolic disorders and cardiac arrhythmias
Federico, Marilén
CaMKII
diabetes
metabolic syndrome
heart
title_short CaMKII: A link between metabolic disorders and cardiac arrhythmias
title_full CaMKII: A link between metabolic disorders and cardiac arrhythmias
title_fullStr CaMKII: A link between metabolic disorders and cardiac arrhythmias
title_full_unstemmed CaMKII: A link between metabolic disorders and cardiac arrhythmias
title_sort CaMKII: A link between metabolic disorders and cardiac arrhythmias
dc.creator.none.fl_str_mv Federico, Marilén
Valverde, Carlos Alfredo
Gonano, Luis Alberto
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author Federico, Marilén
author_facet Federico, Marilén
Valverde, Carlos Alfredo
Gonano, Luis Alberto
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author_role author
author2 Valverde, Carlos Alfredo
Gonano, Luis Alberto
Palomeque, Julieta
Mattiazzi, Ramona Alicia
author2_role author
author
author
author
dc.subject.none.fl_str_mv CaMKII
diabetes
metabolic syndrome
heart
topic CaMKII
diabetes
metabolic syndrome
heart
purl_subject.fl_str_mv https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
dc.description.none.fl_txt_mv The prevalence of metabolic diseases -such as obesity, prediabetes, metabolic syndrome or diabetes-has increased globally over the years. These diseases, mainly diabetes mellitus (DM), are among the leading causes of mortality and morbidity worldwide, with increased risk of diabetic cardiomyopathy (DC), cardiac arrhythmias, and heart failure (HF).In metabolic diseases several steps and proteins involved in excitation-contraction coupling (ECC) are compromised, precluding an efficient and rhythmic cardiac contraction; moreover, calcium/calmodulin-dependent protein kinase II (CaMKII) a kinase involved in ECC, is upregulated in several metabolic maladies and significantly contributes to cardiac remodeling and arrhythmias, among which are calcium (Ca2+)-triggered arrhythmias. CaMKII activation is canonically produced by an increase and binding of Ca2+-calmodulin followed by auto-phosphorylation; furthermore, it may occur as a result of several post-translational modifications, including oxidation and O-GlcNAcylation that are usually present in metabolic illnesses and support chronic CaMKII upregulation and ECC impairment.The aim of the present review is to summarize what is known about the different pathways modifying CaMKII activity and Ca2+ handling in metabolic disorders and may promote Ca2+-triggered arrhythmias even at the early stages of metabolic alterations. Future challenges in this field may encompass unraveling the precise mechanisms by which metabolic disturbances modulate CaMKII activity and its downstream effects on cardiac electrophysiology among different species. This would allow the development of robust and valid preclinical human models that can accurately recapitulate the pathophysiology of the human heart. Additionally, investigating the impact of targeted interventions, such as pharmacological inhibitors or gene therapies, could provide valuable insights into the feasibility and efficacy of manipulating CaMKII signaling to prevent or treat arrhythmias in metabolic disorders.
Fil: Federico, Marilén. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Valverde, Carlos Alfredo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Gonano, Luis Alberto. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Palomeque, Julieta. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
Fil: Mattiazzi, Ramona Alicia. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani". Universidad Nacional de La Plata. Facultad de Ciencias Médicas. Centro de Investigaciones Cardiovasculares "Dr. Horacio Eugenio Cingolani"; Argentina
description The prevalence of metabolic diseases -such as obesity, prediabetes, metabolic syndrome or diabetes-has increased globally over the years. These diseases, mainly diabetes mellitus (DM), are among the leading causes of mortality and morbidity worldwide, with increased risk of diabetic cardiomyopathy (DC), cardiac arrhythmias, and heart failure (HF).In metabolic diseases several steps and proteins involved in excitation-contraction coupling (ECC) are compromised, precluding an efficient and rhythmic cardiac contraction; moreover, calcium/calmodulin-dependent protein kinase II (CaMKII) a kinase involved in ECC, is upregulated in several metabolic maladies and significantly contributes to cardiac remodeling and arrhythmias, among which are calcium (Ca2+)-triggered arrhythmias. CaMKII activation is canonically produced by an increase and binding of Ca2+-calmodulin followed by auto-phosphorylation; furthermore, it may occur as a result of several post-translational modifications, including oxidation and O-GlcNAcylation that are usually present in metabolic illnesses and support chronic CaMKII upregulation and ECC impairment.The aim of the present review is to summarize what is known about the different pathways modifying CaMKII activity and Ca2+ handling in metabolic disorders and may promote Ca2+-triggered arrhythmias even at the early stages of metabolic alterations. Future challenges in this field may encompass unraveling the precise mechanisms by which metabolic disturbances modulate CaMKII activity and its downstream effects on cardiac electrophysiology among different species. This would allow the development of robust and valid preclinical human models that can accurately recapitulate the pathophysiology of the human heart. Additionally, investigating the impact of targeted interventions, such as pharmacological inhibitors or gene therapies, could provide valuable insights into the feasibility and efficacy of manipulating CaMKII signaling to prevent or treat arrhythmias in metabolic disorders.
publishDate 2023
dc.date.none.fl_str_mv 2023-12
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/255843
Federico, Marilén; Valverde, Carlos Alfredo; Gonano, Luis Alberto; Palomeque, Julieta; Mattiazzi, Ramona Alicia; CaMKII: A link between metabolic disorders and cardiac arrhythmias; Elsevier; Aspects of Molecular Medicine; 2; 12-2023; 1-11
2949-6888
CONICET Digital
CONICET
url http://hdl.handle.net/11336/255843
identifier_str_mv Federico, Marilén; Valverde, Carlos Alfredo; Gonano, Luis Alberto; Palomeque, Julieta; Mattiazzi, Ramona Alicia; CaMKII: A link between metabolic disorders and cardiac arrhythmias; Elsevier; Aspects of Molecular Medicine; 2; 12-2023; 1-11
2949-6888
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://linkinghub.elsevier.com/retrieve/pii/S2949688823000229
info:eu-repo/semantics/altIdentifier/doi/10.1016/j.amolm.2023.100022
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-nd/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Elsevier
publisher.none.fl_str_mv Elsevier
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
_version_ 1842269693013917696
score 13.13397

Publicaciones similares