Cell-specific effects of Nox2 on the acute and chronic response to myocardial infarction
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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.

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