Cargando…

Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart

Ca(2+) plays a crucial role in excitation-contraction coupling in cardiac myocytes. Dysfunctional Ca(2+) regulation alters the force of contraction and causes cardiac arrhythmias. Ca(2+) entry into cardiomyocytes is mediated mainly through L-type Ca(2+) channels, leading to the subsequent Ca(2+) rel...

Descripción completa

Detalles Bibliográficos
Autores principales: Zaveri, Sahil, Srivastava, Ujala, Qu, Yongxia Sarah, Chahine, Mohamed, Boutjdir, Mohamed
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10070707/
https://www.ncbi.nlm.nih.gov/pubmed/37025382
http://dx.doi.org/10.3389/fphys.2023.1144069
_version_ 1785019051811012608
author Zaveri, Sahil
Srivastava, Ujala
Qu, Yongxia Sarah
Chahine, Mohamed
Boutjdir, Mohamed
author_facet Zaveri, Sahil
Srivastava, Ujala
Qu, Yongxia Sarah
Chahine, Mohamed
Boutjdir, Mohamed
author_sort Zaveri, Sahil
collection PubMed
description Ca(2+) plays a crucial role in excitation-contraction coupling in cardiac myocytes. Dysfunctional Ca(2+) regulation alters the force of contraction and causes cardiac arrhythmias. Ca(2+) entry into cardiomyocytes is mediated mainly through L-type Ca(2+) channels, leading to the subsequent Ca(2+) release from the sarcoplasmic reticulum. L-type Ca(2+) channels are composed of the conventional Ca(v)1.2, ubiquitously expressed in all heart chambers, and the developmentally regulated Ca(v)1.3, exclusively expressed in the atria, sinoatrial node, and atrioventricular node in the adult heart. As such, Ca(v)1.3 is implicated in the pathogenesis of sinoatrial and atrioventricular node dysfunction as well as atrial fibrillation. More recently, Ca(v)1.3 de novo expression was suggested in heart failure. Here, we review the functional role, expression levels, and regulation of Ca(v)1.3 in the heart, including in the context of cardiac diseases. We believe that the elucidation of the functional and molecular pathways regulating Ca(v)1.3 in the heart will assist in developing novel targeted therapeutic interventions for the aforementioned arrhythmias.
format Online
Article
Text
id pubmed-10070707
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-100707072023-04-05 Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart Zaveri, Sahil Srivastava, Ujala Qu, Yongxia Sarah Chahine, Mohamed Boutjdir, Mohamed Front Physiol Physiology Ca(2+) plays a crucial role in excitation-contraction coupling in cardiac myocytes. Dysfunctional Ca(2+) regulation alters the force of contraction and causes cardiac arrhythmias. Ca(2+) entry into cardiomyocytes is mediated mainly through L-type Ca(2+) channels, leading to the subsequent Ca(2+) release from the sarcoplasmic reticulum. L-type Ca(2+) channels are composed of the conventional Ca(v)1.2, ubiquitously expressed in all heart chambers, and the developmentally regulated Ca(v)1.3, exclusively expressed in the atria, sinoatrial node, and atrioventricular node in the adult heart. As such, Ca(v)1.3 is implicated in the pathogenesis of sinoatrial and atrioventricular node dysfunction as well as atrial fibrillation. More recently, Ca(v)1.3 de novo expression was suggested in heart failure. Here, we review the functional role, expression levels, and regulation of Ca(v)1.3 in the heart, including in the context of cardiac diseases. We believe that the elucidation of the functional and molecular pathways regulating Ca(v)1.3 in the heart will assist in developing novel targeted therapeutic interventions for the aforementioned arrhythmias. Frontiers Media S.A. 2023-03-21 /pmc/articles/PMC10070707/ /pubmed/37025382 http://dx.doi.org/10.3389/fphys.2023.1144069 Text en Copyright © 2023 Zaveri, Srivastava, Qu, Chahine and Boutjdir. https://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
Zaveri, Sahil
Srivastava, Ujala
Qu, Yongxia Sarah
Chahine, Mohamed
Boutjdir, Mohamed
Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title_full Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title_fullStr Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title_full_unstemmed Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title_short Pathophysiology of Ca(v)1.3 L-type calcium channels in the heart
title_sort pathophysiology of ca(v)1.3 l-type calcium channels in the heart
topic Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10070707/
https://www.ncbi.nlm.nih.gov/pubmed/37025382
http://dx.doi.org/10.3389/fphys.2023.1144069
work_keys_str_mv AT zaverisahil pathophysiologyofcav13ltypecalciumchannelsintheheart
AT srivastavaujala pathophysiologyofcav13ltypecalciumchannelsintheheart
AT quyongxiasarah pathophysiologyofcav13ltypecalciumchannelsintheheart
AT chahinemohamed pathophysiologyofcav13ltypecalciumchannelsintheheart
AT boutjdirmohamed pathophysiologyofcav13ltypecalciumchannelsintheheart