First, the dual role of mitophagy in lung diseases remains paradoxical: while adequate mitophagy suppresses NLRP3 inflammasome activation (such as PINK1-mediated mtROS clearance in sepsis), excessive removal of mitochondria (as seen in hyperactive Parkin models) depletes cellular energy reserves, exacerbating epithelial apoptosis. Here, PRKN is linked to Sepsis.