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The downregulation of PRKN in lung epithelial cells of COPD patients may contribute to the deficiency in mitophagy observed in these patients, leading to the accumulation of aberrant mitochondria and increased oxidative stress within cells ( In vitro experiments have suggested that even low levels of PINK1 expression can be compensated by increased PRKN expression, leading to induced mitophagy and reduction of cellular ROS stress during CS exposure, a major risk factor for COPD (Mizumura et al

Early treatment can fully reverse the damage