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.
Highlights
The heart rate of a healthy adult ranges between 60 and 100 beats/min, which is mainly achieved by adequate function of the cardiac contraction/relaxation cycle
This review focuses on the role of Transient receptor potential canonical (TRPC) channels and provides an overview of the most relevant and recent findings related to these channels and ischemia-related disease in the heart
This study revealed that cardiac myocytes treated for 24 h with aldosterone enhance SOCE through the activation of mineralocorticoid receptor, and increase the store-operated Ca2+ current (ISOC ), which correlates with specific overexpression of TRPC1 and 5, as well as stromal interaction molecule 1 (STIM1), but not of
Summary
The heart rate of a healthy adult ranges between 60 and 100 beats/min, which is mainly achieved by adequate function of the cardiac contraction/relaxation cycle. Other players emerged as key partners in the regulation of cardiac Ca2+ handling Among these partners are the transient receptor potential (TRP) channels that are classified in a superfamily, including 28 mammalian TRP proteins divided according their genetic and functional homology into six families: TRPP (polycystin), TRPV (vanilloid), TRPM (melastatin), TRPA (ankyrin), TRPML (mucolipin), and TRPC (canonical). Most TRP channels lack a voltage sensor, they can be activated by physical or biochemical changes, regulating Ca2+ dynamics by directly conducting Ca2+ or prompting Ca2+ entry secondary to membrane depolarization and modulation of voltage-gated Ca2+ channels [5]. The activation mechanism of TRPC channels is not yet completely clarified, and even less so in cardiac cells. Previous studies using different cell types suggest that TRPCs can interact physically with different splice variants of the inositol triphosphate receptors (IP3R). TRPC4 and 5 channels become sensitive to DAG when their interactions with other regulators are inhibited, such as protein kinase C (PKC) and Na+ /H+ exchanger regulatory factor (NHERF) [26]
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