李新桃, 李树壮. 瞬时受体电位C通道与心肌肥厚的研究进展[J]. 心脏杂志, 2016, 28(6): 719-722.
    引用本文: 李新桃, 李树壮. 瞬时受体电位C通道与心肌肥厚的研究进展[J]. 心脏杂志, 2016, 28(6): 719-722.
    Research progress on transient receptor potential canonical channels and cardiac hypertrophy[J]. Chinese Heart Journal, 2016, 28(6): 719-722.
    Citation: Research progress on transient receptor potential canonical channels and cardiac hypertrophy[J]. Chinese Heart Journal, 2016, 28(6): 719-722.

    瞬时受体电位C通道与心肌肥厚的研究进展

    Research progress on transient receptor potential canonical channels and cardiac hypertrophy

    • 摘要: 瞬时受体电位C(transient receptor potential canonical,TRPC)通道作为一类重要的非选择性阳离子通道,在心脏具有广泛的分布和表达。TRPC通道通过改变细胞膜电位和介导钙离子(Ca2+)内流对心脏的生理和病理反应产生重要影响。细胞内Ca2+不仅在心肌细胞的兴奋-收缩偶联中发挥重要作用,而且与各类心脏疾病发生密切相关。最近研究发现,TRPC通道可以通过调节细胞内Ca2+变化,与钙调磷酸酶(calcineurin,CaN)和活化的T细胞核因子(nuclear factor of activated T cells,NFAT)等效应因子参与心肌肥厚的发生发展过程,同时可诱导其他心脏疾病(如心肌纤维化、心率失常、心力衰竭)的发生。本文根据相关研究,围绕TRPC通道在心肌肥厚及相关心脏疾病的发生发展中的作用进行总结回顾。

       

      Abstract: Transient receptor potential canonical (TRPC) channels, as a type of nonselective cation channels, are widely distributed and expressed in the heart. The significance of cardiac TRPC channels is likely connected to the alternation of membrane potential and Ca2+ into a microdomain compartment, which plays a critical role in physiological and pathological responses of the heart. Ca2+ not only involves in the excitation-contraction coupling but also induces the expression of genes responsible for various cardiac diseases. Recently, new evidence has demonstrated that TRPC channel may play a specific role in the development of cardiac hypertrophy through regulating the alteration of intercellular Ca2+ and coordinating with signaling effectors such as calcineurin (CaN) and nuclear factor of activated T cells (NFAT) and may also trigger cardiac diseases such as cardiac fibrosis, arrhythmia and heart failure. In this paper we review the research progress on the role of TRPC channels in cardiac hypertrophy and other heart diseases.

       

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