Fig. 4: CKmito replacement rescues ATP deficiency in mtCaMKII hearts.
From: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
a Western blots and b summary data for CKmito expression normalized to CoxIV from WT (n = 5) and mtCaMKII (n = 5) hearts. c Western blots and d summary data for CK-M expression normalized to α-actinin from WT (n = 5) and mtCaMKII (n = 5) hearts. e Western blot and f summary data for CKmito expression normalized to VDAC1 from WT (n = 7), CKmito (n = 7), mtCaMKII (n = 7), and mtCaMKII x CKmito (n = 6) hearts. g In vivo ATP (left) and PCr (right) quantification from 31P MR spectroscopy in WT (n = 9), CKmito (n = 7), mtCaMKII (n = 8), and mtCaMKII x CKmito (n = 7) hearts. h Summary data for diastolic [Ca2+] measurements made with Fura-2-loaded ventricular myocytes stimulated at 1, 3, and 5 Hz (WT n = 12; CKmito n = 17; mtCaMKII n = 15; mtCaMKII x CKmito n = 13 ventricular myocytes isolated from 2 hearts/group). i Summary data from in vivo MRI measurements in WT (n = 9), CKmito (n = 7), mtCaMKII (n = 8), and mtCaMKII x CKmito (n = 7) hearts. g–i WT and mtCaMKII data are the same as in Fig. 3. j Western blot and k summary data for CaMKII normalized to VDAC1 in mitochondrial lysates from mtCaMKII (n = 3) and mtCaMKII x CKmito (n = 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.
