Fig. 3: mtCaMKII hearts are ATP deficient.
From: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
a ATP content in mitochondria isolated from WT (n = 9) and mtCaMKII (n = 9) hearts. b Example MRI images and corresponding 31P MR spectra and c summary data for ATP and creatine phosphate (PCr) quantification from in vivo 31P MR spectroscopy in WT (n = 9) and mtCaMKII (n = 8) hearts. d Summary data from MRI measurements of WT (n = 9) and mtCaMKII (n = 8) hearts; see Supplementary Movie 1 for MR Cines. e Example intracellular [Ca2+] signals recorded from Fura-2 and f summary data for diastolic (resting) [Ca2+] from isolated ventricular myocytes stimulated at 1, 3, or 5 Hz (WT n = 12; WT+ATP n = 14; mtCaMKII n = 15; mtCaMKII+ATP n = 19) (WT cells were isolated from 2 heart, mtCaMKII cells were isolated from 3 hearts). Data are represented as mean ± SEM, significance was determined using a two-tailed Student’s t test or one-way ANOVA with Tukey’s multiple comparisons test. ****P < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05. Source data, including exact p values, are provided as a Source data file.
