CELL CALCIUM, ONCOGENES, AND HYPERTROPHY
CELL CALCIUM, ONCOGENES, AND HYPERTROPHY
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DOI：
10.1161/01.hyp.15.6.652
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发表时间：
1990-06-01
期刊：
影响因子：
8.3
通讯作者：
KORETSUNE, Y
中科院分区：
文献类型：
--
作者：
MARBAN, E;KORETSUNE, Y
尽管从各种实验方法中收集到诱人的线索，但心脏肥大的细胞机制仍不清楚。在这里，我们研究了细胞质游离Ca2+浓度（[Ca2+]i）的增加触发原癌基因的表达的假设，这反过来又指导了蛋白质合成的特征性增加。来自灌注雪貂心脏的新结果表明，[Ca2+]i增加是灌注压力升高的直接后果。因此，[Ca2+]i在高血压肥厚的初始刺激（灌注压升高）和基因表达的继发性改变之间构成关键联系似乎是合理的。然而，需要进一步的研究来确定[Ca2+]i的变化是否必要或足以刺激心肌细胞生长。
The cellular mechanisms of cardiac hypertrophy remain unclear despite tantalizing clues gleaned from a variety of experimental approaches. Here we examine the hypothesis that an increase in cytosolic free Ca2+ concentration ([Ca2+]i) triggers the expression of proto-oncogenes, which in turn direct the characteristic increase in protein synthesis. New results from perfused ferret hearts are presented demonstrating that [Ca2+]i increases as a direct consequence of an elevation in perfusion pressure. It therefore seems plausible that [Ca2+]i constitutes the crucial link between the initial stimulus for hypertensive hypertrophy (elevated perfusion pressure) and the secondary alterations in gene expression. Nevertheless, further investigation will be required to establish whether changes in [Ca2+]i are necessary or sufficient to stimulate myocardial cell growth.