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. 2020 Dec 15;9:e60827. doi: 10.7554/eLife.60827

Figure 1. SS-31 alleviates the excessive mitochondrial proton leak of cardiomyocytes from 24 mo old mice.

(A) Representative Seahorse assay traces of cardiomyocytes isolated from untreated young and old mice, then exposed or not to 100 nM SS-31 for 2 hr in vitro. Aging-increased basal respiration (C), which was attributable to the augmentation of proton leak (B), but did not affect maximal respiration (D). ANT1 inhibitors Bongkrekic acid (BKA, 10 μM) and carboxyatractyloside (CAT, 20 μM) 2 hr treatment decreased the proton leak (B) and basal respiration (C) but also decreased maximal respiration (D) in old cardiomyocytes. N = 5–14 mice in each group; one-way ANOVA followed by Fisher’s LSD test. *p<0.05, **p<0.01 vs young; #p<0.05, ##p<0.01 vs old controls.

Figure 1.

Figure 1—figure supplement 1. SS-31 has a minor effect on mitochondrial respiration in the young cardiomyocytes.

Figure 1—figure supplement 1.

None of the differences are significant. N = 5 mice in each group. Student’s t-test was applied to determine the statistical significance.
Figure 1—figure supplement 2. SS-31 reaches its inhibitory effect on proton leak suppression at low concentrations.

Figure 1—figure supplement 2.

SS-31 decreased the mitochondrial proton leak. N = 6–14 mice in each group. **p<0.01 vs young, #p<0.05 vs old controls. One-way ANOVA with Fisher’s LSD test was applied.