Calcium in the heart: when it's good, it's very very good, but when it's bad, it's horrid

被引:19
|
作者
Roderick, H. L. [1 ]
Higazi, D. R.
Smyrnias, I.
Fearnley, C.
Harzheim, D.
Bootman, M. D.
机构
[1] Univ Cambridge, Dept Pharmacol, Cambridge CB2 1PD, England
[2] Babraham Inst, Mol Signalling Lab, 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
calcium flux; cardiac failure; cardiac myocyte; contraction; decompensated hypertrophy; heart disease;
D O I
10.1042/BST0350957
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
Ca2+ increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca2+ signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca2+ signalling capacity and cardiac output are reduced. Here, the role that Ca2+ plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca2+ fluxes will be discussed.
引用
收藏
页码:957 / 961
页数:5
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