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The other side of cardiac Ca(2+) signaling: transcriptional control

Ca(2+) is probably the most versatile signal transduction element used by all cell types. In the heart, it is essential to activate cellular contraction in each heartbeat. Nevertheless Ca(2+) is not only a key element in excitation-contraction coupling (EC coupling), but it is also a pivotal second...

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Autores principales: Domínguez-Rodríguez, Alejandro, Ruiz-Hurtado, Gema, Benitah, Jean-Pierre, Gómez, Ana M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508405/
https://www.ncbi.nlm.nih.gov/pubmed/23226134
http://dx.doi.org/10.3389/fphys.2012.00452
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author Domínguez-Rodríguez, Alejandro
Ruiz-Hurtado, Gema
Benitah, Jean-Pierre
Gómez, Ana M.
author_facet Domínguez-Rodríguez, Alejandro
Ruiz-Hurtado, Gema
Benitah, Jean-Pierre
Gómez, Ana M.
author_sort Domínguez-Rodríguez, Alejandro
collection PubMed
description Ca(2+) is probably the most versatile signal transduction element used by all cell types. In the heart, it is essential to activate cellular contraction in each heartbeat. Nevertheless Ca(2+) is not only a key element in excitation-contraction coupling (EC coupling), but it is also a pivotal second messenger in cardiac signal transduction, being able to control processes such as excitability, metabolism, and transcriptional regulation. Regarding the latter, Ca(2+) activates Ca(2+)-dependent transcription factors by a process called excitation-transcription coupling (ET coupling). ET coupling is an integrated process by which the common signaling pathways that regulate EC coupling activate transcription factors. Although ET coupling has been extensively studied in neurons and other cell types, less is known in cardiac muscle. Some hints have been found in studies on the development of cardiac hypertrophy, where two Ca(2+)-dependent enzymes are key actors: Ca(2+)/Calmodulin kinase II (CaMKII) and phosphatase calcineurin, both of which are activated by the complex Ca(2+)/Calmodulin. The question now is how ET coupling occurs in cardiomyocytes, where intracellular Ca(2+) is continuously oscillating. In this focused review, we will draw attention to location of Ca(2+) signaling: intranuclear ([Ca(2+)](n)) or cytoplasmic ([Ca(2+)](c)), and the specific ionic channels involved in the activation of cardiac ET coupling. Specifically, we will highlight the role of the 1,4,5 inositol triphosphate receptors (IP(3)Rs) in the elevation of [Ca(2+)](n) levels, which are important to locally activate CaMKII, and the role of transient receptor potential channels canonical (TRPCs) in [Ca(2+)](c), needed to activate calcineurin (Cn).
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spelling pubmed-35084052012-12-05 The other side of cardiac Ca(2+) signaling: transcriptional control Domínguez-Rodríguez, Alejandro Ruiz-Hurtado, Gema Benitah, Jean-Pierre Gómez, Ana M. Front Physiol Physiology Ca(2+) is probably the most versatile signal transduction element used by all cell types. In the heart, it is essential to activate cellular contraction in each heartbeat. Nevertheless Ca(2+) is not only a key element in excitation-contraction coupling (EC coupling), but it is also a pivotal second messenger in cardiac signal transduction, being able to control processes such as excitability, metabolism, and transcriptional regulation. Regarding the latter, Ca(2+) activates Ca(2+)-dependent transcription factors by a process called excitation-transcription coupling (ET coupling). ET coupling is an integrated process by which the common signaling pathways that regulate EC coupling activate transcription factors. Although ET coupling has been extensively studied in neurons and other cell types, less is known in cardiac muscle. Some hints have been found in studies on the development of cardiac hypertrophy, where two Ca(2+)-dependent enzymes are key actors: Ca(2+)/Calmodulin kinase II (CaMKII) and phosphatase calcineurin, both of which are activated by the complex Ca(2+)/Calmodulin. The question now is how ET coupling occurs in cardiomyocytes, where intracellular Ca(2+) is continuously oscillating. In this focused review, we will draw attention to location of Ca(2+) signaling: intranuclear ([Ca(2+)](n)) or cytoplasmic ([Ca(2+)](c)), and the specific ionic channels involved in the activation of cardiac ET coupling. Specifically, we will highlight the role of the 1,4,5 inositol triphosphate receptors (IP(3)Rs) in the elevation of [Ca(2+)](n) levels, which are important to locally activate CaMKII, and the role of transient receptor potential channels canonical (TRPCs) in [Ca(2+)](c), needed to activate calcineurin (Cn). Frontiers Media S.A. 2012-11-28 /pmc/articles/PMC3508405/ /pubmed/23226134 http://dx.doi.org/10.3389/fphys.2012.00452 Text en Copyright © 2012 Domínguez-Rodríguez, Ruiz-Hurtado, Benitah and Gómez. http://www.frontiersin.org/licenseagreement This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in other forums, provided the original authors and source are credited and subject to any copyright notices concerning any third-party graphics etc.
spellingShingle Physiology
Domínguez-Rodríguez, Alejandro
Ruiz-Hurtado, Gema
Benitah, Jean-Pierre
Gómez, Ana M.
The other side of cardiac Ca(2+) signaling: transcriptional control
title The other side of cardiac Ca(2+) signaling: transcriptional control
title_full The other side of cardiac Ca(2+) signaling: transcriptional control
title_fullStr The other side of cardiac Ca(2+) signaling: transcriptional control
title_full_unstemmed The other side of cardiac Ca(2+) signaling: transcriptional control
title_short The other side of cardiac Ca(2+) signaling: transcriptional control
title_sort other side of cardiac ca(2+) signaling: transcriptional control
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3508405/
https://www.ncbi.nlm.nih.gov/pubmed/23226134
http://dx.doi.org/10.3389/fphys.2012.00452
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