In conclusion, ApN retains its beneficial properties in dystrophic muscles by activating AdipoR1 and the AMPK-SIRT1-PGC-1α pathway, thereby inducing a shift in the secretion of downstream myokines toward a less inflammatory profile while upregulating utrophin A. ApN as well as its downstream myokines may be therapeutic targets for the management of DMD. This evidence concerns the gene SIRT1 and Duchenne muscular dystrophy.