2026-06-14T03:46:21Zhttps://repisalud.isciii.es/rest/oai/request

oai:repisalud.isciii.es:20.500.12105/252832024-10-23T13:07:24Zcom_20.500.12105_15322com_20.500.12105_2051col_20.500.12105_16958col_20.500.12105_16963

00925njm 22002777a 4500 dc Falcón, Débora author Galeano-Otero, Isabel author Martín-Bórnez, Marta author Fernández-Velasco, María author Gallardo-Castillo, Isabel author Rosado, Juan A author Ordóñez, Antonio author Smani, Tarik author 2020-01-10 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. 10.3390/cells9010173 2073-4409 Cells http://hdl.handle.net/10668/14954 31936700 https://hdl.handle.net/20.500.12105/25283 Ca2+ entry TRPC channel Cardiac infarction Cardiac repair TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease.