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European Heart Journal 1990 11(Supplement G):1-7; doi:10.1093/eurheartj/11.suppl_G.1
Copyright © 1990 by the European Society of Cardiology.
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© 1990 The European Society of Cardiology

Biological signals of cardiac hypertrophy

J. L. Samuel, I. Dubus, F. Contard, K. Schwartz and L. Rappaport

U 127 INSERM, Hopital Lariboisière Paris, France

Address for correspondence: L. Rappaport, INSERM U127, Hopital Lariboisière, 41 bd de la chapelle 75010 Paris, France

Chronic increases in haemodynamic load modify the expression of cardiac genes, leading to a new phenotype better adapted to the new functional demand. Several mechanisms such as the global activation of genes, the modulation of single genes and / or differential expression of multigene families may account for these modifications. Changes in gene expression of isomyosin shift are permanent and have been associated with modifications of the physiological properties of cardiac muscle. The exact cellular and molecular mechanisms which either do or do not initiate and maintain these changes in cardiac expression remain to be elucidated. Recent technical advances in cellular and molecular biology provide a foundation for understanding those cellular mechanisms that control cardiac muscle growth. This is a review of some transient changes in gene expression induced by mechanical overload such as the expression of cellular oncogenes, heat shock protein and {alpha}-skeletal actin genes. The biological functions of these genes are not yet precisely defined, some of them could interfere in the process of myocyte hypertrophy.

Key Words: Myocyte hypertrophy • gene expression • triggers


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