Angiotensin-converting　enzyme　2　(ACE2)　has　been　reported　to　exert　a　protective　effect　in　acute　lung　injury　(ALI),　though　its　underlying　mechanism　remains　incompletely　understood.　In　this　study,　ACE2　expression　was　found　to　be　upregulated　in　a　mouse　model　of　ALI　induced　by　lipopolysaccharide　(LPS)　injection.　ACE2　knockdown　modulated　the　severity　of　ALI,　the　extent　of　autophagy,　and　the　mTOR　pathway　in　this　model.　ACE2　regulated　liver　kinase　B1　(LKB1)　gene　expression　by　sequestering　miR-326,　thereby　alleviating　ALI　severity　through　enhanced　autophagy.　In　cell-based　experiments,　miR-326　was　shown　to　regulate　ACE2　and　LKB1　expression　and　autophagy.　Overexpression　of　ACE2　disrupted　miR-326＇s　regulatory　effect　on　LKB1,　suggesting　that　LKB1　may　function　as　an　endogenous　sponge　for　miR-326.　These　findings　imply　that　elevated　ACE2　expression　in　lung　could　play　enhance　the　autophagy　via　the　consumption　of　miR-326.