Role of Reactive Oxygen Species in the Regulation of Cardiac Myocyte Phenotype

摘要

Summary. In cardiac myocytes in vitro, ROS can cause either hypertrophy or apoptosis in a concentration-dependent manner with hypertrophy in response to low levels of ROS and apoptosis in response to*higher levels. Likewise, there is evidence that ROS mediate the hypertrophic effects of ct-adrenergic receptor stimulation and low-level mechanical strain, and the apoptotic effects of P-adrenergic receptor stimulation or higher amplitude mechanical strain. The MAPK signaling pathway appears to mediate several of these effects of ROS. Erk is involved in the hypertrophic response to low levels of ROS, low amplitude mechanical strain and cc-adrenergic receptor stimulation. In' contrast, JNK is involved in the apoptotic effect of higher levels of ROS, high amplitude mechanical strain and P-adrenergic receptor stimulation. These observations indicate that ROS play a critical role in the determination of myocyte phenotype in response to a variety of stimuli associated with cellular growth or death.