Control of cardiac gene expression by mechanical stress.

Cardiac growth can be divided into two categories: normal growth in the developmental process and cardiac hypertrophy induced by hemodynamic overload. Since cardiac myocytes are terminally differentiated and lose their ability to duplicate soon after birth, they respond to increased workload only by an increase in cell size (hypertrophy), not by an increase in cell number (hyperplasia). Moreover, the induction of specific gene expression is observed in cardiac hypertrophy. Cardiac hypertrophy induced by hemodynamic overload has two important aspects. The first is a medical issue. Cardiac hypertrophy and the resulting heart failure due to valvular disease and hypertension are one of the main causes of mortality and morbidity in humans. Although cardiac hypertrophy by a chronic overload per se is not a pathological but rather a physiological response of the heart to pathological states, heart failure as a final form of hypertrophy is an obvious disease. To know the mechanisms of cardiac hypertrophy by overload might pave the way to understand the mechanisms of heart failure. The second aspect of cardiac hypertrophy is of biological interest. Cardiac myocytes respond to overload not only by an increase in cell volume, but also by altered expressions of specific genes. The myocardium has an extraordinary plasticity at the biochemical level as well as at the physiological level, and the regulation of gene expression is dynamic in the heart. There are many examples that show external physical (mechanical) stimuli to have significant effects on