Preprint Review Version 1 Preserved in Portico This version is not peer-reviewed

TRPC channels: Dysregulation and Ca2+ Mishandling In Ischemic Heart Disease

Version 1 : Received: 24 December 2019 / Approved: 25 December 2019 / Online: 25 December 2019 (09:23:14 CET)

A peer-reviewed article of this Preprint also exists.

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. 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.

Journal reference: Cells 2020, 9, 173
DOI: 10.3390/cells9010173

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, TRPC may form homo or heterotetrameric ion channel, 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 of the expression of different TRPC isoforms has been observed in different animal model of heart infarcts, and in vitro experimental model of ischemia and reperfusion. TRPC-mediated increase of the intracellular Ca2+ concentration seems required for the activation of 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 will highlight the current knowledge regarding TRPC implication in different cellular processes related to ischemia and reperfusion, and to heart infarction.

Subject Areas

trpc channel; ca2+ entry; cardiac infarction; cardiac repair

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