瞬时受体电位通道蛋白C与肺动脉高压

doi:10.3969/j.issn.2095-3755.2017.03.000

结核病与肺部健康杂志 ›› 2017, Vol. 6 ›› Issue (3): 279-293.doi: 10.3969/j.issn.2095-3755.2017.03.000

瞬时受体电位通道蛋白C与肺动脉高压

徐磊,付秀华

010050 内蒙古医科大学附属医院呼吸与危重症医学科

收稿日期:2017-03-27 出版日期:2017-09-30 发布日期:2017-09-30
作者简介:付秀华

Transient receptor potential channels proteins and the pathogenesis of pulmonary hypertension

XU Lei, FU Xiu-hua

Department of Respiratory and Critical Care Medicine, the Affiliated Hospital of Inner Mongolia Medical University, Hohhot 010050, China

Received:2017-03-27 Online:2017-09-30 Published:2017-09-30

摘要/Abstract

摘要： 肺动脉高压致死致残率高，是一种严重威胁人类健康疾病，对其发病机制的研究非常重要。在肺动脉高压发病机制中，肺血管平滑肌细胞内Ca2+浓度的增加是核心因素，Ca2+浓度的增加会引起细胞的增殖进而引起肺动脉高压。细胞内Ca2+浓度主要受细胞膜Ca2+通道的调节，瞬时受体电位通道蛋白C是Ca2+通道蛋白的主要成分。瞬时受体电位通道蛋白C1、4、6参与了肺动脉高压的发病，笔者对其具体机制进行了综述。

Abstract: Pulmonary hypertension is one of the diseases that seriously threaten to human health with significant mortality and disability rate. It is vital to explore the mechanism of pathogenesis of pulmonary hypertension for its prevention and treatment. The increase in Ca2+ concentration of pulmonary artery smooth muscles cells enhances cell proliferation and consequent causes occurrence of pulmonary hypertension, which plays a core role in the pathogenesis of pulmonary hypertension. The Ca2+ concentration of cells is regulated by calcium channels on cell membrane. The transient receptor potential channel C (TRPC) is the main component of calcium channels, and TRPC1/4/6 are involved in pathogenesis of pulmonary hypertension. In the present article, we reviewed the pathogenesis of pulmonary hypertension in detail.

徐磊,付秀华. 瞬时受体电位通道蛋白C与肺动脉高压[J]. 结核病与肺部健康杂志, 2017, 6(3): 279-293. doi: 10.3969/j.issn.2095-3755.2017.03.000

XU Lei, FU Xiu-hua. Transient receptor potential channels proteins and the pathogenesis of pulmonary hypertension[J]. Journal of Tuberculosis and Lung Health, 2017, 6(3): 279-293. doi: 10.3969/j.issn.2095-3755.2017.03.000

参考文献

[1] Opitz C, Rosenkranz S, Ghofrani HA, et al. ESC guidelines 2015 pulmonary hypertension: diagnosis and treatment. Dtsch Med Wochenschr, 2016, 141(24): 1764-1769.
[2] Wieder N, Greka A. Calcium,TRPC channels, and regulation of the actin cytoskeleton in podocytes: towards a future of targeted therapies. Pediatr Nephrol, 2016, 31(7): 1047-1054.
[3] Zhang H, Li W, Xue Y, et al. TRPC1 is involved in Ca2+ influx and cytotoxicity following Pb2+ exposure in human embryonic kidney cells. Toxicol lett, 2014, 229(1): 52-58.
[4] Banner KH, Igney F, Poll C. TRP channels: emerging targets for respiratory disease. Pharmacol Ther, 2011, 130(3): 371-384.
[5] Lai N, Lu W, Wang J. Ca2+ and ion channels in hypoxia-mediated pulmonary hypertension. Int J Clin Exp Pathol, 2015, 8(2): 1081-1092.
[6] Nesin V, Tsiokas L. Trpc1. Handb Exp Pharmacol, 2014, 222: 15-51.
[7] Xia Y, Yang XR, Fu Z, et al. Classical transient receptor potential 1 and 6 contribute to hypoxic pulmonary hypertension through differential regulation of pulmonary vascular functions. Hypertension, 2014, 63(1): 173-180.
[8] Liu XR, Zhang MF, Yang N, et al. Enhanced store-operated Ca2+ entry and TRPC channel expression in pulmonary arteries of monocrotaline-induced pulmonary hypertensive rats. Am J Physiol Cell Physiol, 2012, 302(1): C77-C87.
[9] Lu W, Ran P, Zhang D, et al. Sildenafil inhibits chronically hypoxic upregulation of canonical transient receptor potential expression in rat pulmonary arterial smooth muscle. Am J Physiol Cell Physiol, 2010, 298(1): C114-C123.
[10] Sun CK, Zhen YY, Lu HI, et al. Reducing TRPC1 expression through liposome-mediated siRNA delivery markedly attenuates hypoxia-induced pulmonary arterial hypertension in a murine model. Stem Cells Int, 2014, 2014:316214.
[11] Zhang S, Remillard CV, Fantozzi I, et al. ATP-induced mitogenesis is mediated by cyclic AMP response element-binding protein-enhanced TRPC4 expression and activity in human pulmonary artery smooth muscle cells. Am J Physiol Cell Physiol, 2004, 287(5): C1192-C1201.
[12] Tsvilovskyy VV, Zholos AV, Aberle T, et al. Deletion of TRPC4 and TRPC6 in mice impairs smooth muscle contraction and intestinal motility in vivo. Gastroenterology, 2009, 137(4): 1415-1424.
[13] Tiruppathi C, Freichel M, Vogel SM, et al. Impairment of store-operated Ca2+ entry in TRPC4-/- mice interferes with increase in lung microvascular permeability. Circ Res, 2002, 91(1): 70-76.
[14] Alzoubi A, Almalouf P, Toba M, et al. TRPC4 inactivation confers a survival benefit in severe pulmonary arterial hypertension. Am J Pathol, 2013, 183(6): 1779-1788.
[15] Weissmann N, Dietrich A, Fuchs B, et al. Classical transient receptor potential channel 6 (TRPC6) is essential for hypoxic pulmonary vasoconstriction and alveolar gas exchange. Proc Natl Acad Sci U S A, 2006, 103(50): 19093-19098.
[16] Wang J, Weigand L, Lu W, et al. Hypoxia inducible factor 1 mediates hypoxia-induced TRPC expression and elevated intracellular Ca2+ in pulmonary arterial smooth muscle cells. Circ Res, 2006, 98(12): 1528-1537.
[17] Wang J, Jiang Q, Wan L, et al. Sodium tanshinone IIA sulfonate inhibits canonical transient receptor potential expression in pulmonary arterial smooth muscle from pulmonary hypertensive rats. Am J Respir Cell Mol Biol, 2013, 48(1): 125-134.
[18] Lin XH, Hong HS, Zou GR, et al. Upregulation of TRPC1/6 may be involved in arterial remodeling in rat. J Surg Res, 2015, 195(1): 334-343.
[19] Zhang J, Lu W, Chen Y, et al. Bortezomib alleviates experimental pulmonary hypertension by regulating intracellular calcium homeostasis in PASMCs. Am J Physiol Cell Physiol, 2016, 311(3): C482-C497.
[20] Peng G, Lu W, Li X, et al. Expression of store-operated Ca2+ entry and transient receptor potential canonical and vanilloid-related proteins in rat distal pulmonary venous smooth muscle. Am J Physiol Lung Cell Mol Physiol, 2010, 299(5): L621-L630.
[21] Xu L, Chen Y, Yang K, et al. Chronic hypoxia increases TRPC6 expression and basal intracellular Ca2+ concentration in rat distal pulmonary venous smooth muscle. PloS One, 2014, 9(11): e112007.
[22] Wang Q, Wang D, Yan G, et al. TRPC6 is required for hypoxia-induced basal intracellular calcium concentration elevation, and for the proliferation and migration of rat distal pulmonary venous smooth muscle cells. Mol Med Rep, 2016, 13(2): 1577-1585.

瞬时受体电位通道蛋白C与肺动脉高压

Transient receptor potential channels proteins and the pathogenesis of pulmonary hypertension

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