Calcium signalling remodelling and disease

被引:282
作者
Berridge, Michael J. [1 ]
机构
[1] Babraham Inst, Cambridge CB22 3AT, England
基金
英国生物技术与生命科学研究理事会;
关键词
Alzheimer's disease; bipolar disorder; calcium; heart; inositol; schizophrenia; INOSITOL 1,4,5-TRISPHOSPHATE RECEPTORS; ALZHEIMERS-DISEASE; UP-REGULATION; CA2+; RELEASE; DYSREGULATION; OSCILLATIONS; HYPERTROPHY; CONTRACTION; ARRHYTHMIAS;
D O I
10.1042/BST20110766
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
A wide range of Ca2+ signalling systems deliver the spatial and temporal Ca2+ signals necessary to control the specific functions of different cell types. Release of Ca2+ by InsP(3) (inositol 1,4,5-trisphosphate) plays a central role in many of these signalling systems. Ongoing transcriptional processes maintain the integrity and stability of these cell-specific signalling systems. However, these homoeostatic systems are highly plastic and can undergo a process of phenotypic remodelling, resulting in the Ca2+ signals being set either too high or too low. Such subtle dysregulation of Ca2+ signals have been linked to some of the major diseases in humans such as cardiac disease, schizophrenia, bipolar disorder and Alzheimer's disease.
引用
收藏
页码:297 / 309
页数:13
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