Involvement of TRP channels in the cardiac hypertrophy and cell death

在心肌肥厚模型中，TRPC1、-C3、-C6、脑利钠肽(BNP)表达增加，NFAT活性、钙内流增加，细胞表面积增加。基因沉默的TRPC1和药物治疗的吡唑衍生物或西地那非减少钙内流，防止心肌肥厚。在对基质相互作用分子1(STIM1；被称为细胞内钙存储的钙感受器)基因敲除小鼠的分析中，我们提供了STIM1和TRPC1在心肌肥厚发生发展中起关键作用的证据。此外，在压力超负荷条件下，STIM1参与了心肌纤维化的形成。最终，TRPC/STIM1系统可能成为治疗心肌肥厚的新的药理靶点。

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.