Fig. 3: Pharmacological inhibition of the mitochondrial F0F1 ATP synthase triggers hypermetabolism. | Communications Biology

Fig. 3: Pharmacological inhibition of the mitochondrial F0F1 ATP synthase triggers hypermetabolism.

From: OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases

Fig. 3

a Schematic of the study design for fibroblast profiling across the lifespan from three Control donors treated with 1 nM Oligomycin (Oligo). b Lifespan trajectories of JATP (Glycolytic + OxPhos) derived from oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) obtained from Seahorse measurements across the cells’ lifespan (up to 150 days). Percentages show the total average difference between Oligo and Control. c Balance of JATP derived from OxPhos and glycolysis across the lifespan and d oligo-induced metabolic shift. Dotted lines denote the range in control cells. e Relative average lifespan energy expenditure by cell line normalized to control, f corrected for cell volume. g Average of proton leak and h coupling efficiency measures on the Seahorse normalized to control. i Lifespan trajectories and j average mtDNA copy number at the first three time points (early life) and peak value across the lifespan. n = 3 individuals per group, 7–9 timepoints per individual. Data are means ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, mixed effects model for Oligo vs. control.

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