TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease

Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and the...

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Main Authors: Débora Falcón, Isabel Galeano-Otero, Marta Martín-Bórnez, María Fernández-Velasco, Isabel Gallardo-Castillo, Juan A. Rosado, Antonio Ordóñez, Tarik Smani
Format: Article
Language:English
Published: MDPI AG 2020-01-01
Series:Cells
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Online Access:https://www.mdpi.com/2073-4409/9/1/173
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author Débora Falcón
Isabel Galeano-Otero
Marta Martín-Bórnez
María Fernández-Velasco
Isabel Gallardo-Castillo
Juan A. Rosado
Antonio Ordóñez
Tarik Smani
author_facet Débora Falcón
Isabel Galeano-Otero
Marta Martín-Bórnez
María Fernández-Velasco
Isabel Gallardo-Castillo
Juan A. Rosado
Antonio Ordóñez
Tarik Smani
author_sort Débora Falcón
collection DOAJ
description Transient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca<sup>2+</sup> concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.
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spelling doaj.art-33c46d8de08e416994dd7849f8a2d2362023-09-02T23:22:46ZengMDPI AGCells2073-44092020-01-019117310.3390/cells9010173cells9010173TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart DiseaseDébora Falcón0Isabel Galeano-Otero1Marta Martín-Bórnez2María Fernández-Velasco3Isabel Gallardo-Castillo4Juan A. Rosado5Antonio Ordóñez6Tarik Smani7Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, SpainDepartment of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, SpainDepartment of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, SpainBiomedical Research Networking Centers of Cardiovascular Diseases (CIBERCV), 28029 Madrid, SpainDepartment of Stomatology, School of Dentistry, University of Seville, 41009 Seville, SpainDepartment of Physiology (Cell Physiology Research Group), Institute of Molecular Pathology Biomarkers, University of Extremadura, 10003 Caceres, SpainBiomedical Research Networking Centers of Cardiovascular Diseases (CIBERCV), 28029 Madrid, SpainDepartment of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, SpainTransient receptor potential canonical (TRPC) channels are ubiquitously expressed in excitable and non-excitable cardiac cells where they sense and respond to a wide variety of physical and chemical stimuli. As other TRP channels, TRPC channels may form homo or heterotetrameric ion channels, and they can associate with other membrane receptors and ion channels to regulate intracellular calcium concentration. Dysfunctions of TRPC channels are involved in many types of cardiovascular diseases. Significant increase in the expression of different TRPC isoforms was observed in different animal models of heart infarcts and in vitro experimental models of ischemia and reperfusion. TRPC channel-mediated increase of the intracellular Ca<sup>2+</sup> concentration seems to be required for the activation of the signaling pathway that plays minor roles in the healthy heart, but they are more relevant for cardiac responses to ischemia, such as the activation of different factors of transcription and cardiac hypertrophy, fibrosis, and angiogenesis. In this review, we highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion and to heart infarction.https://www.mdpi.com/2073-4409/9/1/173trpc channelca<sup>2+</sup> entrycardiac infarctioncardiac repair
spellingShingle Débora Falcón
Isabel Galeano-Otero
Marta Martín-Bórnez
María Fernández-Velasco
Isabel Gallardo-Castillo
Juan A. Rosado
Antonio Ordóñez
Tarik Smani
TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
Cells
trpc channel
ca<sup>2+</sup> entry
cardiac infarction
cardiac repair
title TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
title_full TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
title_fullStr TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
title_full_unstemmed TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
title_short TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
title_sort trpc channels dysregulation and ca sup 2 sup mishandling in ischemic heart disease
topic trpc channel
ca<sup>2+</sup> entry
cardiac infarction
cardiac repair
url https://www.mdpi.com/2073-4409/9/1/173
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