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|本期目录/Table of Contents|

瞬时受体电位C通道与心肌肥厚的研究进展

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2016年第6期
页码:
719-722
栏目:
综述
出版日期:
2016-07-05

文章信息/Info

Title:
Research progress on transient receptor potential canonical channels and cardiac hypertrophy
作者:
李新桃李树壮
(大连医科大学生理学教研室,辽宁 大连 116044)
Author(s):
LI Xin-tao LI Shu-zhuang
(Department of Physiology, Dalian Medical University, Dalian 116044, Liaoning, China)
关键词:
瞬时受体电位C通道钙离子信号通路心肌肥厚心脏疾病
Keywords:
TRPC channel Ca2+ signal pathway cardiac hypertrophy heart disease
分类号:
R542.2
DOI:
-
文献标识码:
A
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.

参考文献/References

[1]Ambudkar IS,Bandyopadhyay BC,Liu X,et al.Functional organization of TRPC-Ca2+ channels and regulation of calcium microdomains[J].Cell calcium,2006,40(5-6):495-504.
[2]Watanabe H,Iino K,Ohba T,et al.Possible involvement of TRP channels in cardiac hypertrophy and arrhythmia[J].Curr Top Med Chem,2013,13(3):283-294.
[3]Montell C,Rubin GM.Molecular characterization of the Drosophila trp locus:a putative integral membrane protein required for phototransduction[J].Neuron,1989,2(4):1313-1323.
[4]Hardie RC,Minke B.The trp gene is essential for a light-activated Ca2+ channel in Drosophila photoreceptors[J].Neuron,1992,8(4):643-651.
[5]Dietrich A,Kalwa H,Rost BR,et al.The diacylgylcerol-sensitive TRPC3/6/7 subfamily of cation channels: functional characterization and physiological relevance[J].Pflugers Arch,2005,451(1):72-80.
[6]Yue Z,Xie J,Yu AS,et al.Role of TRP channels in the cardiovascular system[J].Am J Physiol Heart Circ Physiol,2015,308(3):H157-H182.
[7]Maroto R,Raso A,Wood TG,et al.TRPC1 forms the stretch-activated cation channel in vertebrate cells[J].Nat Cell Biol,2005,7(2):179-185.
[8]Spassova MA,Hewavitharana T,Xu W,et al.A common mechanism underlies stretch activation and receptor activation of TRPC6 channels[J].Proc Natl Acad Sci U S A,2006,103(44):16586-16591.
[9]Watanabe H,Murakami M,Ohba T,et al.The pathological role of transient receptor potential channels in heart disease[J].Circ J,2009,73(3):419-427.
[10]Jiang Y,Huang H,Liu P,et al.Expression and localization of TRPC proteins in rat ventricular myocytes at various developmental stages[J].Cell Tissue Res,2014,355(1):201-212.
[11]Seth M,Zhang ZS,Mao L,et al.TRPC1 channels are critical for hypertrophic signaling in the heart[J].Circ Res,2009,105(10):1023-1030.
[12]Nakayama H,Wilkin BJ,Bodi I,et al.Calcineurin-dependent cardiomyopathy is activated by TRPC in the adult mouse heart[J].FASEB J,2006,20(10):1660-1670.
[13]Wu X,Eder P,Chang B,et al.TRPC channels are necessary mediators of pathologic cardiac hypertrophy[J].Proc Natl Acad Sci U S A,2010,107(15) 7000-7005.
[14]Ohba T,Watanabe H,Murakami M,et al.Upregulation of TRPC1 in the development of cardiac hypertrophy[J].J Mol Cell Cardiol,2007,42(3):498-507.
[15]Wang P,Liu D,Tepel M,et al.Transient receptor potential canonical type 3 channels--their evolving role in hypertension and its related complications[J].J Cardiovasc Pharmacol,2013,61(6):455-460.
[16]Eder P,Probst D,Rosker C,et al.Phospholipase C-dependent control of cardiac calcium homeostasis involves a TRPC3-NCX1 signaling complex[J].Cardiovasc Res,2007,73(1):111-119.
[17]Ong HL,de Souza LB,Cheng KT,et al.Physiological functions and regulation of TRPC channels[J]. Handb Exp Pharmacol,2014,223:1005-1034.
[18]Cooley N,Grubb DR,Luo J,et al.The phosphatidylinositol(4,5)bisphosphate-binding sequence of transient receptor potential channel canonical 4alpha is critical for its contribution to cardiomyocyte hypertrophy[J].Mol Pharmacol,2014,86(4):399-405.
[19]Onohara N,Nishida M,Inoue R,et al.TRPC3 and TRPC6 are essential for angiotensin II-induced cardiac hypertrophy[J].EMBO J,2006,25(22):5305-5316.
[20]Xie J,Cha SK,An SW,et al.Cardioprotection by Klotho through downregulation of TRPC6 channels in the mouse heart[J].Nat Commun,2012,3:1238.
[21]Koitabashi N,Aiba T,Hesketh GG,et al.Cyclic GMP/PKG-dependent inhibition of TRPC6 channel activity and expression negatively regulates cardiomyocyte NFAT activation Novel mechanism of cardiac stress modulation by PDE5 inhibition[J].J Mol Cell Cardiol,2010,48(4):713-724.
[22]Nishida M,Watanabe K,Sato Y,et al.Phosphorylation of TRPC6 channels at Thr69 is required for anti-hypertrophic effects of phosphodiesterase 5 inhibition[J].J Biol Chem,2010,285(17):13244-13253.
[23]Seo K,Rainer PP,Shalkey Hahn V,et al.Combined TRPC3 and TRPC6 blockade by selective small-molecule or genetic deletion inhibits pathological cardiac hypertrophy[J].Proc Natl Acad Sci U S A,2014,111(4):1551-1556.
[24]Harada M,Luo X,Qi XY,et al.Transient receptor potential canonical-3 channel-dependent fibroblast regulation in atrial fibrillation[J].Circulation,2012,126(17):2051-2064.
[25]Ward ML,Williams IA,Chu Y,et al.Stretch-activated channels in the heart:contributions to length-dependence and to cardiomyopathy[J].Prog Biophys Mol Biol,2008,97(2-3):232-249.
[26]Bush EW,Hood DB,Papst PJ,et al.Canonical transient receptor potential channels promote cardiomyocyte hypertrophy through activation of calcineurin signaling[J].J Biol Chem,2006,281(44):33487-33496.
[27]Kuwahara K, Wang Y, McAnally J, et al. TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling[J].J Clin Invest,2006,116(12):3114-3126.
[28]Satoh S,Tanaka H,Ueda Y,et al.Transient receptor potential(TRP)protein 7 acts as a G protein-activated Ca2+ channel mediating angiotensin II-induced myocardial apoptosis[J].Mol Cell Biochem,2007,294(1-2):205-215.

备注/Memo

备注/Memo:
收稿日期:2015-08-24.
通讯作者:李树壮,教授,主要从事循环系统的损伤与保护研究Email:shuzhuangli@126.com
作者简介:李新桃,本科生Email:xintaoli1992@126.com
更新日期/Last Update: 2016-07-10