Physiology and pathophysiology of canonical transient receptor potential channels

被引:267
作者
Abramowitz, Joel [1 ]
Birnbaumer, Lutz [1 ]
机构
[1] NIEHS, Transmembrane Signaling Grp, Neurobiol Lab, NIH,Dept Hlth & Human Serv, Res Triangle Pk, NC 27709 USA
关键词
calcium; cardiovascular system; epithelium; lung; neuron; CAPACITATIVE CA2+ ENTRY; ARTERIAL SMOOTH-MUSCLE; METABOTROPIC GLUTAMATE RECEPTORS; CA2+-PERMEABLE CATION CHANNEL; INTESTINAL EPITHELIAL-CELLS; NECROSIS-FACTOR-ALPHA; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTOR; CALCIUM-INDUCED DIFFERENTIATION; GLOMERULAR MESANGIAL CELLS; CHRONIC LITHIUM TREATMENT;
D O I
10.1096/fj.08-119495
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The existence of a mammalian family of TRPC ion channels, direct homologues of TRP, the visual transduction channel of flies, was discovered during 1995-1996 as a consequence of research into the mechanism by which the stimulation of the receptor-Gq-phospholipase C beta signaling pathway leads to sustained increases in intracellular calcium. Mammalian TRPs, TRPCs, turned out to be nonselective, calcium-permeable cation channels, which cause both a collapse of the cell's membrane potential and entry of calcium. The family comprises 7 members and is widely expressed. Many cells and tissues express between 3 and 4 of the 7 TRPCs. Despite their recent discovery, a wealth of information has accumulated, showing that TRPCs have widespread roles in almost all cells studied, including cells from excitable and nonexcitable tissues, such as the nervous and cardiovascular systems, the kidney and the liver, and cells from endothelia, epithelia, and the bone marrow compartment. Disruption of TRPC function is at the root of some familial diseases. More often, TRPCs are contributing risk factors in complex diseases. The present article reviews what has been uncovered about physiological roles of mammalian TRPC channels since the time of their discovery. This analysis reveals TRPCs as major and unsuspected gates of Ca2+ entry that contribute, depending on context, to activation of transcription factors, apoptosis, vascular contractility, platelet activation, and cardiac hypertrophy, as well as to normal and abnormal cell proliferation. TRPCs emerge as targets for a thus far nonexistent field of pharmacological intervention that may ameliorate complex diseases. - Abramowitz, J., Birnbaumer, L. Physiology and pathophysiology of canonical transient receptor potential channels. FASEB J. 23, 297 - 328 ( 2009)
引用
收藏
页码:297 / 328
页数:32
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