Here, we showed that ascorbic acid treatment of cultured COPD myotubes reduced myotube atrophy and decreased the expression of FoxO1, MuRF1 and atrogin-1, whereas the pro-oxidant molecule H2O2 led to increased atrophy with upregulation of MuRF1 and FoxO1 expression. This evidence concerns the gene TRIM63 and chronic obstructive pulmonary disease.