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

  • Melanie Maytin
  • Douglas B. Sawyer
  • Wilson S. Colucci
Part of the Progress in Experimental Cardiology book series (PREC, volume 10)


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 α-adrenergic receptor stimulation and low-level mechanical strain, and the apoptotic effects of β-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 α-adrenergic receptor stimulation. In contrast, JNK is involved in the apoptotic effect of higher levels of ROS, high amplitude mechanical strain and β-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.

Key words

cardiac myocytes phenotype apoptosis hypertrophy reactive oxygen species 


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Copyright information

© Springer Science+Business Media Dordrecht 2004

Authors and Affiliations

  • Melanie Maytin
    • 1
  • Douglas B. Sawyer
    • 1
  • Wilson S. Colucci
    • 1
  1. 1.Cardiovascular Medicine Section, Department of MedicineBoston University Medical Center and the Myocardial Biology Unit, Boston University School of MedicineBostonUSA

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