Effect of hepatocyte growth factor and angiotensin II on rat cardiomyocyte hypertrophy

Chen, Ai-Lan; Ou, Cai-Wen; He, Zhao-Chu; Liu, Qi-Cai; Dong, Qi; Chen, Min-Sheng

Myocardial hypertrophy is defined as a thickening of the myocardium, which results in a decrease in the size of the chamber of the heart, including the left and right ventricles, and is an important risk factor for subsequent cardiac morbidity and mortality. The pathophysiology and role of cardiomyocyte hypertrophy in heart disease have been intensively investigated; however, to date they are only partially understood. Cardiac hypertrophic growth is the primary responsive mechanism by which the heart reduces stress on the ventricular wall. Conventional views suggest that cardiomyocyte hypertrophy is a compensatory response to increased hemodynamic overload, which leads to cardiac disease. However, recent findings in genetic animal models of myocardial hypertrophy as well as human studies have revealed support for a molecular basis whereby either compensatory or maladaptive forms of hypertrophy exist, and only the latter lead to cardiac failure (1) . In the case of myocardial infarction, hypertrophic responses occur in cardiomyocytes in the surviving portion of the ventricle, and ventricular dilatation follows as a result of re-organization of the myocardium, including cardiomyocytes and mesenchymal cells in combination (2, 3) . To execute this response, the cardiomyocytes are stimulated by neurohumoral factors and subsequent intracellular reactive cascade systems. All of these processes entail an increase in protein synthesis as well as the size and architectural rearrangement within individual cardiomyocytes.