瞬时受体电位通道C亚族参与高血压心室肥厚机制研究的新进展

心肌肥厚的发生及逆转一直是心血管病研究的热点。传统观点认为Ca^2＋超载是心肌肥厚发生的基础。近年的相关研究提示瞬时受体电位通道C亚族（Transient receptor potential channels,TRPC）可能通过调节细胞内Ca2＋变化而参与心肌肥厚的发生发展过程。也有新的证据表明TRPC通道参与并调节心室肥厚过程主要是通过TRPC通道本身的激活与调节,心脏微结构域的作用及钙调神经磷酸酶（calcineurin,CaN）、活化的T细胞核因子（nuclear factor of activated T cells,NFAT）等信号传导效应因子间相互协调的信号传导实现的。TRPC通道可能成为阻止和逆转心室肥厚的药物作用新靶点。

New progress of the study on the effect and mechanism of TRPC channels in the development of hypertension induced ventricular hypertrophy

The development and reversal of myocardial hypertrophy is always as a hot spot in the study of cardiovascular disease. Traditionally, Ca2+ overload is seen as the foundation of myocardial hypertrophy. Recent years, related studies found transient receptor potential channels (TRPC) may play a certain role in the development of myocardial hypertrophy through adjusting the alteration of intracellular Ca2+ . Besides, new evidences have demonstrated the regulating effect of TRPC channels in ventricular hypertrophy mainly achieves through the activation and self regulation of TRPC channels, the effect of microdomain in the heart and the coordination with signaling effectors such as calcineurin and NFAT (nuclear factor of activated T cells). TRPC channels may become a new pharmacological target on the inhibition and reversal of ventricular hypertrophy.