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机械应力对心脏基因的调节。癌基因信号传导假说。

Modulation of cardiac genes by mechanical stress. The oncogene signalling hypothesis.

作者信息

Schneider M D, Roberts R, Parker T G

机构信息

Department of Medicine, Baylor College of Medicine, Houston, TX 77030.

出版信息

Mol Biol Med. 1991 Apr;8(2):167-83.

PMID:1839641
Abstract

In cardiac muscle, the selectivity and specificity of gene regulation by heparin-binding and transforming growth factors resembles the characteristic program of fetal gene induction during myocardial hypertrophy produced by load. Shared by isolated cardiac myocytes and intact hearts, these complex and heterogeneous responses provide intriguing systems, which are distinct from other lineages and models of cell growth, for the study of trophic signal transduction by cellular oncogenes. A functional role for peptide growth factors and other oncogene-encoded proteins in myocardial hypertrophy suggests biological pathways which might usefully be exploited to promote compensatory growth following infarction or to interfere with maladaptive changes during a hemodynamic load.

摘要

在心肌中,肝素结合因子和转化生长因子对基因调控的选择性和特异性,类似于负荷所致心肌肥大过程中胎儿基因诱导的特征性程序。这些复杂而异质性的反应在分离的心肌细胞和完整心脏中都存在,为研究细胞癌基因的营养信号转导提供了有趣的系统,该系统不同于其他细胞生长谱系和模型。肽生长因子和其他癌基因编码蛋白在心肌肥大中发挥功能性作用,提示了一些生物学途径,这些途径可能有助于促进梗死灶后的代偿性生长,或干扰血流动力学负荷期间的适应性改变。

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