Cigarette　smoke-induced　airway　epithelial　cell　mitophagy　is　an　important　mechanism　in　the　pathogenesis　of　chronic　obstructive　pulmonary　disease　(COPD).　Mitochondrial　protein　Nix　(also　known　as　BNIP3L)　is　a　selective　autophagy　receptor　and　participates　in　several　human　diseases.　However,　little　is　known　about　the　role　of　Nix　in　airway　epithelial　cell　injury　during　the　development　of　COPD.　The　aim　of　the　present　study　is　to　investigate　the　effects　of　Nix　on　mitophagy　and　mitochondrial　function　in　airway　epithelial　cells　exposed　to　cigarette　smoke　extract　(CSE).　Our　present　study　has　found　that　CSE　could　increase　Nix　protein　expression　and　induce　mitophagy　in　airway　epithelial　cells.　And　Nix　siRNA　significantly　inhibited　mitophagy　and　attenuated　mitochondrial　dysfunction　and　cell　injury　when　airway　epithelial　cells　were　stimulated　with　7.5%　CSE.　In　contrast,　Nix　overexpression　enhanced　mitophagy　and　aggravated　mitochondrial　dysfunction　and　cell　injury　when　airway　epithelial　cells　were　incubated　with　7.5%　CSE.　These　data　suggest　that　Nix-dependent　mitophagy　promotes　airway　epithelial　cell　and　mitochondria　injury　induced　by　cigarette　smoke,　and　may　be　involved　in　the　pathogenesis　of　COPD　and　other　cigarette　smoke-associated　diseases.