AKT1 and myocardial infarction: During myocardial ischemia-reperfusion (I/R), cardiomyocyte NOX4 levels contributed to macrophage proliferation and polarization responses, and volume overload improved ventricular remodeling after myocardial infarction (MI) through NOX4 activation of Akt and an increase in downstream protein synthesis markers (S6 ribosomal protein and eIF4E-BP1), a therapeutic target (70).