ROS contribute to adverse cardiac remodeling after myocardial infarction (MI).
Nox2 is a major cardiac ROS source but with cell-specific effects.
Increased Nox2 in cardiomyocytes augments hypertrophy and fibrosis post-MI.
Increased Nox2 in endothelium has no significant effect on cardiac remodeling after MI.
Cardiomyocyte Nox2 may have the more important role in post-MI remodeling.