Fig. 4

Plin5 deficiency increased NADH levels in cardiomyocytes. A, B The myocardia of wild-type (Plin5^+/+) and Plin5-knockout (Plin5^−/−) mice were observed by transmission electron microscopy, and the numbers of mitochondria were statistically analysed (n = 3, **P < 0.01). C Quantification of mitochondrial DNA in the myocardium of Plin5^+/+ and Plin5^−/− mice (n = 3, *P < 0.05). D Representative images and quantification analysis of MitoTracker staining of primary cardiomyocytes from Plin5^+/+ and Plin5^−/− mice with or without FAs) stimulation. Scale bar, 10 μM (n = 3, *P < 0.05, **P < 0.01). E Western blotting and quantitive analysis of CPT1, CPT2 and PGC-1α in primary cardiomyocytes from Plin5^+/+ and Plin5^−/− mice (n = 3, *P < 0.05, **P < 0.01). F NADH levels and NAD+/NADH ratios in myocardia Plin5^+/+ and Plin5^−/− mice (n = 3, **P < 0.01). G NADH levels and NAD+/NADH ratios in primary wild-type (Plin5^+/+) and Plin5-null (Plin5.^−/−) cardiomyocytes in the absence and presence of FAs (n = 3, *P < 0.05, **P < 0.01). H NADH levels and NAD + /NADH ratios in Plin5-overexpressing H9C2 cells after treatment with or without FAs (n = 3, *P < 0.05, **P < 0.01)