Involvement of TRP channels in the cardiac hypertrophy and cell death

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In cardiac hypertrophy model, we could detect increases in the expression of TRPC1,-C3, -C6, brain natriuretic peptide (BNP), and NFAT activity, Ca entry, as well as increases in cell surface area. Gene silencing of the TRPC1 and pharmacological treatment with a pyrazole derivative or sildenafil attenuate the Ca entry and prevent cardiac hypertrophy. In analysis of stromal interaction molecule 1 (STIM1; known as a Ca sensor of intracellular Ca store) knockout mice, we provide evidence that STIM1 together with TRPC1 is crucial for the development of cardiac hypertrophy. Moreover, STIM1 contributes to cardiac fibrosis under the condition of pressure over load. Ultimately, TRPC/STIM1 system might become novel pharmacological target in the treatment of cardiac hypertrophy.