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Overview
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Background
Pyr3, a pyrazole compound, selectively inhibits the canonical transient receptor potential channel 3 (TRPC3) [1].
TRPC3 is a member of TRPCs which control influxes of Ca2+ and other cations that induce diverse cellular processes upon stimulation of plasma membrane receptors coupled to phospholipase C. TRPC3 has been implicated in diverse biological functions, including B cell receptor-mediated Ca2+ oscillations, T cell receptor-dependent Ca2+ entry pathway, and cardiac hypertrophy [1].
In HEK293 cells, Pyr3 selectively inhibited TRPC3-mediated Ca2+ influx in a dose-dependent manner, with an IC50 value of 0.7 μM. In rat neonatal cardiomyocytes, Pyr3 suppressed activation of nuclear factor of activated T cells, with an IC50 value of 0.05 μM [1].
In sham operated mice, chronic treatment with Pyr3 (0.1 mg·kg−1·day−1, i.p.), Pyr3 attenuated in vivo pressure overload-induced cardiac hypertrophy. In addition, the transverse aortic constriction operation-induced increase in expression of atrial natriuretic peptide mRNA, a reliable marker for cardiac hypertrophy, was also suppressed by Pyr3 [1].
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