Unlike previous studies that primarily focused on P4’s role in reproductive health, our study elucidates the mechanisms by which P4 activates the c-MYC/SIRT1/PGC-1α axis, thereby promoting mitochondrial function and reducing oxidative stress, representing a significant advancement in understanding the metabolic and molecular pathways involved in COPD and offering a new avenue for potential treatment strategies. This evidence concerns the gene PPARGC1A and chronic obstructive pulmonary disease.