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TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling

Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressu...

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Autores principales: Falcón, Debora, Galeano-Otero, Isabel, Calderón-Sánchez, Eva, Del Toro, Raquel, Martín-Bórnez, Marta, Rosado, Juan A., Hmadcha, Abdelkrim, Smani, Tarik
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406032/
https://www.ncbi.nlm.nih.gov/pubmed/30881310
http://dx.doi.org/10.3389/fphys.2019.00159
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author Falcón, Debora
Galeano-Otero, Isabel
Calderón-Sánchez, Eva
Del Toro, Raquel
Martín-Bórnez, Marta
Rosado, Juan A.
Hmadcha, Abdelkrim
Smani, Tarik
author_facet Falcón, Debora
Galeano-Otero, Isabel
Calderón-Sánchez, Eva
Del Toro, Raquel
Martín-Bórnez, Marta
Rosado, Juan A.
Hmadcha, Abdelkrim
Smani, Tarik
author_sort Falcón, Debora
collection PubMed
description Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressure-overload, or myocardial injury can cause pathologic hypertrophic growth of the heart followed by interstitial fibrosis. The consequent heart’s structural and molecular adaptation might elevate the risk of developing heart failure and malignant arrhythmia. Compelling evidences have demonstrated that Ca(2+) entry through TRP channels might play pivotal roles in cardiac function and pathology. TRP proteins are classified into six subfamilies: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPP (polycystin), which are activated by numerous physical and/or chemical stimuli. TRP channels participate to the handling of the intracellular Ca(2+) concentration in cardiac myocytes and are mediators of different cardiovascular alterations. This review provides an overview of the current knowledge of TRP proteins implication in the pathologic process of some frequent cardiac diseases associated with the adverse cardiac remodeling such as cardiac hypertrophy, fibrosis, and conduction alteration.
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spelling pubmed-64060322019-03-15 TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling Falcón, Debora Galeano-Otero, Isabel Calderón-Sánchez, Eva Del Toro, Raquel Martín-Bórnez, Marta Rosado, Juan A. Hmadcha, Abdelkrim Smani, Tarik Front Physiol Physiology Calcium is an important second messenger required not only for the excitation-contraction coupling of the heart but also critical for the activation of cell signaling pathways involved in the adverse cardiac remodeling and consequently for the heart failure. Sustained neurohumoral activation, pressure-overload, or myocardial injury can cause pathologic hypertrophic growth of the heart followed by interstitial fibrosis. The consequent heart’s structural and molecular adaptation might elevate the risk of developing heart failure and malignant arrhythmia. Compelling evidences have demonstrated that Ca(2+) entry through TRP channels might play pivotal roles in cardiac function and pathology. TRP proteins are classified into six subfamilies: TRPC (canonical), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPP (polycystin), which are activated by numerous physical and/or chemical stimuli. TRP channels participate to the handling of the intracellular Ca(2+) concentration in cardiac myocytes and are mediators of different cardiovascular alterations. This review provides an overview of the current knowledge of TRP proteins implication in the pathologic process of some frequent cardiac diseases associated with the adverse cardiac remodeling such as cardiac hypertrophy, fibrosis, and conduction alteration. Frontiers Media S.A. 2019-03-01 /pmc/articles/PMC6406032/ /pubmed/30881310 http://dx.doi.org/10.3389/fphys.2019.00159 Text en Copyright © 2019 Falcón, Galeano-Otero, Calderón-Sánchez, Del Toro, Martín-Bórnez, Rosado, Hmadcha and Smani. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Physiology
Falcón, Debora
Galeano-Otero, Isabel
Calderón-Sánchez, Eva
Del Toro, Raquel
Martín-Bórnez, Marta
Rosado, Juan A.
Hmadcha, Abdelkrim
Smani, Tarik
TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title_full TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title_fullStr TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title_full_unstemmed TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title_short TRP Channels: Current Perspectives in the Adverse Cardiac Remodeling
title_sort trp channels: current perspectives in the adverse cardiac remodeling
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6406032/
https://www.ncbi.nlm.nih.gov/pubmed/30881310
http://dx.doi.org/10.3389/fphys.2019.00159
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