2026-06-14T05:18:29Zhttps://repisalud.isciii.es/rest/oai/requestoai: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
Repisalud
author
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
2024-10-23T13:07:24Z
2024-10-23T13:07:24Z
2020-01-10
10.3390/cells9010173
2073-4409
Cells
http://hdl.handle.net/10668/14954
31936700
https://hdl.handle.net/20.500.12105/25283
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.
eng
Ca2+ entry
TRPC channel
Cardiac infarction
Cardiac repair
TRPC Channels: Dysregulation and Ca2+ Mishandling in Ischemic Heart Disease.
research article