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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Ca2+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。
The occurrence and reversal of cardiac hypertrophy has always been the focus of cardiovascular disease research. The traditional view that Ca2 + overload is the basis of cardiac hypertrophy. Recent studies suggest that Transient receptor potential channels (TRPCs) may participate in the development of cardiac hypertrophy by regulating intracellular Ca2 + changes. There is also new evidence that TRPC channels participate in and regulate ventricular hypertrophy through activation and regulation of the TRPC channel itself, effects of cardiac micro-domains and calcineurin (CaN), activated nuclear factor-kappaB of activated T cells, NFAT) and other signaling mediators. TRPC channels may serve as a new target for drug action to prevent and reverse ventricular hypertrophy.