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Review

TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease

by
Débora Falcón
1,2,†,
Isabel Galeano-Otero
1,†,
Marta Martín-Bórnez
1,
María Fernández-Velasco
2,3,
Isabel Gallardo-Castillo
4,
Juan A. Rosado
5,
Antonio Ordóñez
2,* and
Tarik Smani
1,2,*
1
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, Spain
2
Biomedical Research Networking Centers of Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain
3
IdiPAZ Institute for Health Research La PAZ, 28029 Madrid, Spain
4
Department of Stomatology, School of Dentistry, University of Seville, 41009 Seville, Spain
5
Department of Physiology (Cell Physiology Research Group), Institute of Molecular Pathology Biomarkers, University of Extremadura, 10003 Caceres, Spain
*
Authors to whom correspondence should be addressed.
†
Débora Falcón and Isabel Galeano Otero contributed equally to this work.
Cells 2020, 9(1), 173; https://doi.org/10.3390/cells9010173
Submission received: 19 November 2019 / Revised: 3 January 2020 / Accepted: 8 January 2020 / Published: 10 January 2020
(This article belongs to the Special Issue TRPC Channels)
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Abstract

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 Ca2+ 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.
Keywords: TRPC channel; Ca2+ entry; cardiac infarction; cardiac repair TRPC channel; Ca2+ entry; cardiac infarction; cardiac repair

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MDPI and ACS Style

Falcón, D.; Galeano-Otero, I.; Martín-Bórnez, M.; Fernández-Velasco, M.; Gallardo-Castillo, I.; Rosado, J.A.; Ordóñez, A.; Smani, T. TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease. Cells 2020, 9, 173. https://doi.org/10.3390/cells9010173

AMA Style

Falcón D, Galeano-Otero I, Martín-Bórnez M, Fernández-Velasco M, Gallardo-Castillo I, Rosado JA, Ordóñez A, Smani T. TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease. Cells. 2020; 9(1):173. https://doi.org/10.3390/cells9010173

Chicago/Turabian Style

Falcón, Débora, Isabel Galeano-Otero, Marta Martín-Bórnez, María Fernández-Velasco, Isabel Gallardo-Castillo, Juan A. Rosado, Antonio Ordóñez, and Tarik Smani. 2020. "TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease" Cells 9, no. 1: 173. https://doi.org/10.3390/cells9010173

APA Style

Falcón, D., Galeano-Otero, I., Martín-Bórnez, M., Fernández-Velasco, M., Gallardo-Castillo, I., Rosado, J. A., Ordóñez, A., & Smani, T. (2020). TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease. Cells, 9(1), 173. https://doi.org/10.3390/cells9010173

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