Possible Involvement of TRP Channels in Cardiac Hypertrophy and Arrhythmia

被引:1
作者
Watanabe, Hiroyuki [1 ]
Iino, Kenji [1 ]
Ohba, Takayoshi [1 ,2 ]
Ito, Hiroshi
机构
[1] Akita Univ, Grad Sch Med, Dept Cardiovasc & Resp Med, Akita 0108543, Japan
[2] Akita Univ, Grad Sch Med, Dept Physiol, Akita 0108543, Japan
关键词
Cardiac arrhythmia; cardiac hypertrophy; Orai1; Stim1; TRPC1; TRPC3; TRPC6; TRPM4; NONSELECTIVE CATION CHANNEL; OPERATED CA2+ ENTRY; RECEPTOR POTENTIAL CHANNELS; FUNCTIONAL-CHARACTERIZATION; ATRIAL-FIBRILLATION; CHLORIDE CURRENT; NUCLEAR FACTOR; ION-CHANNEL; CALCINEURIN; HEART;
D O I
暂无
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Over the past 20 years, studies of transient receptor potential (TRP) channels have significantly extended our knowledge regarding the molecular basis of Ca2+ signals in cardiac myocytes. The functional significance of cardiac TRP channels is likely connected to the alteration of membrane potential or Ca2+ entry into a noncontractile compartment, where gene expression responsible for various cardiac diseases is induced. This review highlights some aspects of TRP channels with anticipated roles in cardiac disease. Evidence suggests that (a) increased activities of TRPC1, TRPC3, or TRPC6 are involved in the development of cardiac hypertrophy, where these TRPC channels act as unique sensors for a wide range of hypertrophic stimuli, and (b) mutations in TRPM4 are now recognized as causes of human cardiac conduction disorders. Ultimately, TRP channels may become novel pharmacological targets in the treatment of human cardiac disease.
引用
收藏
页码:283 / 294
页数:12
相关论文
共 100 条
[51]   TRPC1 forms the stretch-activated cation channel in vertebrate cells [J].
Maroto, R ;
Raso, A ;
Wood, TG ;
Kurosky, A ;
Martinac, B ;
Hamill, OP .
NATURE CELL BIOLOGY, 2005, 7 (02) :179-U99
[52]   Increased catecholamine secretion contributes to hypertension in TRPM4-deficient mice [J].
Mathar, Ilka ;
Vennekens, Rudi ;
Meissner, Marcel ;
Kees, Frieder ;
Van der Mieren, Gerry ;
Londono, Juan E. Camacho ;
Uhl, Sebastian ;
Voets, Thomas ;
Hummel, Bjoern ;
van den Bergh, An ;
Herijgers, Paul ;
Nilius, Bernd ;
Flockerzi, Veit ;
Schweda, Frank ;
Freichel, Marc .
JOURNAL OF CLINICAL INVESTIGATION, 2010, 120 (09) :3267-3279
[53]   A calcineurin-dependent transcriptional pathway for cardiac hypertrophy [J].
Molkentin, JD ;
Lu, JR ;
Antos, CL ;
Markham, B ;
Richardson, J ;
Robbins, J ;
Grant, SR ;
Olson, EN .
CELL, 1998, 93 (02) :215-228
[54]   The TRP channels, a remarkably functional family [J].
Montell, C ;
Birnbaumer, L ;
Flockerzi, V .
CELL, 2002, 108 (05) :595-598
[55]   Transient receptor potential 1 regulates capacitative Ca2+ entry and Ca2+ release from endoplasmic reticulum in B lymphocytes [J].
Mori, Y ;
Wakamori, M ;
Miyakawa, T ;
Hermosura, M ;
Hara, Y ;
Nishida, M ;
Hirose, K ;
Mizushima, A ;
Kurosaki, M ;
Mori, E ;
Gotoh, K ;
Okada, T ;
Fleig, A ;
Penner, R ;
Iino, M ;
Kurosaki, T .
JOURNAL OF EXPERIMENTAL MEDICINE, 2002, 195 (06) :673-681
[56]   Reverse-remodeling effects of angiotensin II type 1 receptor blocker in a canine atrial fibrillation model [J].
Nakashima, Hideko ;
Kumagai, Koichiro .
CIRCULATION JOURNAL, 2007, 71 (12) :1977-1982
[57]   Calcineurin-dependent cardiomyopathy is activated by TRPC in the adult mouse heart [J].
Nakayama, Hiroyuki ;
Wilkin, Benjamin J. ;
Bodi, Ilona ;
Molkentin, Jeffery D. .
FASEB JOURNAL, 2006, 20 (10) :1660-1670
[58]   MOVEMENTS OF CA IN FROG HEART VENTRICLES AT REST AND DURING CONTRACTURES [J].
NIEDERGERKE, R .
JOURNAL OF PHYSIOLOGY-LONDON, 1963, 167 (03) :515-+
[59]   Voltage dependence of the Ca2+-activated cation channel TRPM4 [J].
Nilius, B ;
Prenen, J ;
Droogmans, G ;
Voets, T ;
Vennekens, R ;
Freichel, M ;
Wissenbach, U ;
Flockerzi, V .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (33) :30813-30820
[60]   Transient receptor potential cation channels in disease [J].
Nilius, Bernd ;
Owsianik, Grzegorz ;
Voets, Thomas ;
Peters, John A. .
PHYSIOLOGICAL REVIEWS, 2007, 87 (01) :165-217