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. 2018 Apr 7;7(8):e007805. doi: 10.1161/JAHA.117.007805

Figure 9.

Figure 9

The alterations of mitochondrial properties in nonischemic heart failure (NI‐HF) mice. A, Fluorescence staining results revealed that the overall mitochondrial mass increased from background‐subtracted normalized fluorescence (F/Fo) of 1.13±0.02 in sham ventricular cardiomyocytes (n=16) to 1.20±0.03 in NI‐HF cardiomyocytes (n=19). B, Compared with sham cardiomyocytes (n=12), the mitochondrial membrane potential was slightly depolarized in NI‐HF cardiomyocytes (n=10). Mitochondrial membrane potential was collapsed by 20 µmol/L carbonyl cyanide 4‐(trifluoromethoxy) phenylhydrazone (FCCP) in both sham and NI‐HF cardiomyocytes. C, Western blots of mitochondrial Ca2+ uniporter (MCU), mitochondrial Na+‐Ca2+ exchange (NCLX), and phosphorylated MCU. D, The expression of phosphorylated MCU was upregulated from 0.30±0.04 in sham group to 1.45±0.46 in NI‐HF group. GFP indicates green fluorescent protein; p‐tyrosine, phosphorylated tyrosine; TMRM, tetramethylrhodamine methyl ester. *P<0.05 compared with that in sham group.