title: Biological signals of cardiac hypertrophy.
abstract: 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.
authors: U 127 INSERM, Hopital Lariboisière, Paris, France.
authors: J L
authors: JL
authors: Samuel
authors: I
authors: I
authors: Dubus
authors: F
authors: F
authors: Contard
authors: K
authors: K
authors: Schwartz
authors: L
authors: L
authors: Rappaport
mesh_terms: D000199:Actins / Q000235:genetics; D000818:Animals; D006332:Cardiomegaly / Q000209:etiology / Q000235:genetics*; D015870:Gene Expression / Q000502:physiology*; D006360:Heat-Shock Proteins / Q000235:genetics; D006801:Humans; D009218:Myosins / Q000235:genetics*; D011519:Proto-Oncogenes / Q000235:genetics*; D012333:RNA, Messenger / Q000235:genetics; D014335:Tropomyosin / Q000235:genetics
chemical_list: D000199:Actins; D006360:Heat-Shock Proteins; D012333:RNA, Messenger; D014335:Tropomyosin; D009218:Myosins