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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
Biol Psychiatry (2011) 69:9123
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Control 15 , 405408 (2006)
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