Dichloroacetate improves mitochondrial function, physiology, and morphology in FBXL4 disease models.

By contrast, DCA treatment of fbxl‐1 ( ok4741 ) worms led to a nonsignificant trend toward increased intracellular lactate levels (73.4% ± 9.6%) relative to untreated fbxl‐1 ( ok4741 ) worms ( Figure 4J ).

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Consistent with FBXL4 –/– disease causing variable degrees of mitochondrial dysfunction, CS activity, used as a proxy for mitochondrial content, showed a trend toward decrease by 51% in fibroblasts from participant 1 (49% ± 12%, mean ± SEM) and was significantly decreased by 56% in fibroblasts from participant 2 (44 ± 11%) when normalized to healthy control human fibroblasts (100% ± 13%) ( Figure 7A ).

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