Figure 8. The OXPHOS‐mediated lipogenic reprogramming is prevented by edaravone.
The schematic illustrates the effect of in vivo edaravone administration in Skm from LowOXPHOS mice. Restraining OXPHOS generates a ROS‐mediated rewiring of lipid metabolism through enhanced BCAA catabolism and lipid synthesis. Skm and WAT perturbations in lipid species are observed, defining a LowOXPHOS phenotype of adiposity and lipotoxicity. Edaravone treatment restores normal ROS and lipid metabolism, reducing v‐WAT deposits and preventing the setting of IR mediated by mitochondrial dysfunction.