Fig. 6: mtCaMKII activates TCA cycle dehydrogenases and augments resting NADH.
From: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
a Pyruvate dehydrogenase (PDH) activity in isolated mitochondria from WT (n = 7) and mtCaMKII (n = 9) hearts. b TCA cycle enzyme activities in permeabilized mitochondria from WT (n = 7) and mtCaMKII (n = 9) hearts, CS: citrate synthase, IDH: isocitrate dehydrogenase, α-KGDH: α-ketoglutarate dehydrogenase, SL: succinate-CoA ligase, SDH: succinate dehydrogenase, MDH: malate dehydrogenase. c Representative NADH imaging of isolated ventricular myocytes before pacing (calibration bar = 50 μm). d Quantification of NADH autofluorescence in isolated ventricular myocytes before and after pacing from WT (n = 29 myocytes from two hearts) and mtCaMKII (n = 52 myocytes from three hearts) hearts. Maximum (100%) NADH was measured in the presence of NaCN, and minimum (0%) in the presence of FCCP. Cells from the same genotype were paired in comparisons of before and after pacing. e Quantification of NAD+ and NADH in hearts from WT (n = 4) and mtCaMKII (n = 4) mice. f Western blot and g summary data for acetylated proteins normalized to VDAC1 in isolated mitochondria from WT (n = 4) and mtCaMKII (n = 4) hearts. Data are represented as mean ± SEM, significance was determined using a two-tailed Student’s t test. ****P < 0.0001, **P < 0.01, *P < 0.05. Source data, including exact p values, are provided as a Source data file.
