TRPC Channels: Dysregulation and Ca<sup>2+</sup> Mishandling in Ischemic Heart Disease
Débora Falcón,
Isabel Galeano-Otero,
Marta Martín-Bórnez,
María Fernández-Velasco,
Isabel Gallardo-Castillo,
Juan A. Rosado,
Antonio Ordóñez,
Tarik Smani
Affiliations
Débora Falcón
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, Spain
Isabel Galeano-Otero
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, Spain
Marta Martín-Bórnez
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, Spain
María Fernández-Velasco
Biomedical Research Networking Centers of Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain
Isabel Gallardo-Castillo
Department of Stomatology, School of Dentistry, University of Seville, 41009 Seville, Spain
Juan A. Rosado
Department of Physiology (Cell Physiology Research Group), Institute of Molecular Pathology Biomarkers, University of Extremadura, 10003 Caceres, Spain
Antonio Ordóñez
Biomedical Research Networking Centers of Cardiovascular Diseases (CIBERCV), 28029 Madrid, Spain
Tarik Smani
Department of Medical Physiology and Biophysics, Institute of Biomedicine of Seville, University of Seville, 41013 Seville, Spain
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.
