[Molecular mechanisms of myocardial hypertrophy and deterioration]

The development of cardiac compensatory hypertrophy (CCH) during heart adaptation to increased load is conditioned by two simultaneous processes which are accelerated synthesis and slower degradation of protein. In CCH, increased protein-synthesizing capacity of the myocardium is based on accelerated transcription. At the same time, the rates of rRNA and mRNA degradation are increased at the emergency stage of CCH. Organ-nonspecific cytoplasmic protein factors are identified that take part in the mechanism which initiates accelerated transcription during CCH. Along with total transcription acceleration, a selective activation of structural genes which code the most effective isoenzymes occurs in the heart at the emergency stage. A standard complex of biochemical changes in myocardial metabolism is shown to occur at the stage of wear and during physiological ageing: RNA concentration is decreased, the rates of its synthesis and degradation are reduced, as are the rates of protein synthesis and degradation. At the same time, administration of tRNA to animals accelerates protein synthesis in such a heart.