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重塑钙离子信号系统与心肌肥大

Remodelling Ca2+ signalling systems and cardiac hypertrophy.

作者信息

Berridge M J

机构信息

The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.

出版信息

Biochem Soc Trans. 2006 Apr;34(Pt 2):228-31. doi: 10.1042/BST20060228.

Abstract

In cardiac cells, Ca2+ signals appear as brief transients responsible for controlling both contraction and transcription. Information may be encoded in these digital signals through changes in both frequency and shape. An increase in Ca2+ signalling contributes to a process of phenotypic remodelling during hypertrophy. The increase in Ca2+ that drives the larger contractions may be responsible for switching on a second process of signalosome remodelling to down-regulate the Ca2+ signalling pathway. It is a change in the properties of the Ca2+ transient that seems to carry the information responsible for the remodelling of the cardiac gene transcription programme that leads first to hypertrophy and then to congestive heart failure.

摘要

在心肌细胞中,Ca2+信号表现为短暂的瞬变,负责控制收缩和转录。信息可能通过频率和形状的变化编码在这些数字信号中。Ca2+信号的增加有助于肥大过程中的表型重塑。驱动更大收缩的Ca2+增加可能负责开启信号体重塑的第二个过程,以下调Ca2+信号通路。似乎是Ca2+瞬变特性的改变携带了负责心脏基因转录程序重塑的信息,该重塑首先导致肥大,然后导致充血性心力衰竭。

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