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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\u2010dependent 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\u2010associated diseases.<\/jats:p>","DOI":"10.1002\/jcp.28117","type":"journal-article","created":{"date-parts":[[2019,1,8]],"date-time":"2019-01-08T22:10:31Z","timestamp":1546985431000},"page":"14210-14220","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":45,"title":["Nix\/BNIP3L\u2010dependent mitophagy accounts for airway epithelial cell injury induced by cigarette smoke"],"prefix":"10.1002","volume":"234","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0794-2546","authenticated-orcid":false,"given":"Ming","family":"Zhang","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine The Second Affiliated Hospital of Xi\u2019an Jiaotong University Xi\u2019an Shaanxi 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