[Phenotype changes in myocardial proteins in hemodynamic overloads].

The phenotype of myocardial proteins is not set once and for all: it changes during ontogenesis, haemodynamic overload and in many other circumstances (e.g. dysthyroidism, diabetes). These changes are attributed either to the differential expression of multigenic protein families, or to modulation of single gene expression. In haemodynamic overload, this versatility of the myocardium enables it, usually by re-expression of its foetal phenotype, to find in itself the capacity for getting adjusted to new functioning conditions. The mechanisms that link the heart work overload to these phenotypic transitions, as well as their possible physiopathology, remain to be determined.