Increased Cardiomyocyte Apoptosis and Changes in Proapoptotic and Antiapoptotic Genes <i>bax</i> and <i>bcl</i> -2 During Left Ventricular Adaptations to Chronic Pressure Overload in the Rat

Abstract

These data suggest that in response to chronic pressure overload, cardiomyocyte-specific apoptosis contributed to the transition from LVH to LVD. LVH and LVD were accompanied by a dramatic cardiomyocyte upregulation of the proapoptotic gene bax and reduced bcl-2/bax ratio, predisposing cardiomyocytes to apoptosis.