This study investigates the role of PINK1-PARK2-mediated mitophagy in regulating cigarette smoke extract-induced mitochondrial damage and cellular senescence in primary human bronchial epithelial cells, revealing that reduced PARK2 expression in COPD lungs contributes to insufficient mitophagy and enhanced oxidative stress, implicating this pathway in COPD pathogenesis. Here, PINK1 is linked to chronic obstructive pulmonary disease.