CAMK2G and left ventricular hypertrophy: The double transgenic mice, combining mitochondrial-targeted CaMKII overexpression and extramitochondrial CaMKII inhibition, showed persistent left ventricular dysfunction (see left ventricular ejection fraction) and dilation (see left ventricular end-systolic and diastolic volumes), but loss of left ventricular hypertrophy (see heart weight/body weight), compared to the mtCaMKII mice (Fig. 2c).