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discovered that, compared with wild-type COPD mice, parkin RBR E3 ubiquitin protein ligase ( PRKN ) gene-knockout mice exhibited a more substantial accumulation of damaged mitochondria, cellular senescence, airway wall thickening, emphysema lesions, and inflammatory response after exposure to CS for 6 months ( In vitro experiments showed that even with reduced PINK1 protein levels, overexpression of PRKN was still capable of inducing mitophagy, effectively reducing mtROS production, and delaying cell senescence