目的 探讨肌管蛋白相关蛋白14（MTMR14）介导的线粒体自噬在慢性阻塞性肺疾病（COPD） 气道炎症中的作用。方法 选择 2020 年 12 月至 2021 年 12 月在本院胸外科因医疗原因接受手术的患者作为研究对象。根据肺功能和吸烟史将受试者分为 2 组：对照组和 COPD 组。通过免疫组化和免疫印迹 检测 MTMR14 在人肺组织中的表达。分别采用香烟烟雾提取物（CSE）处理人气道上皮细胞系 NuLi⁃1 和小 鼠来模拟 COPD，并研究了过表达的 MTMR14 对体外和体内 COPD 模型的影响。结果 与对照组相比， COPD 患者肺部的 MTMR14 表达降低。MTMR14 过表达抑制 CSE 诱导的细胞活力降低、线粒体氧化应激和 炎症，并在体外改善线粒体功能和线粒体自噬。MTMR14 过表达抑制 COPD 小鼠肺部炎症细胞浸润、间质 水肿和充血，并降低血清 IL⁃6 和 IL⁃8 水平。此外，MTMR14 过表达在一定程度上改善了 COPD 小鼠肺组织 线粒体功能，抑制线粒体自噬过度激活。结论 MTMR14 过表达减轻 COPD 的炎症和肺气肿，这在一定程 度上取决于线粒体功能和线粒体自噬的调节。

Objective To investigate the role of myotubulin ⁃ related protein 14（MTMR14）⁃mediated mitophagy in airway inflammation in chronic obstructive pulmonary disease（COPD）. Methods Participants who underwent surgery for medical reasons in the department of thoracic surgery of our hospital from December 2020 to December 2021 were selected and assigned to control and COPD group according to lung function and smoking history. Expression of MTMR14 in human lung tissue was detected by immunohistochemistry and immunoblotting. The human airway epithelial cell line NuLi⁃1 and mice were given cigarette smoke extract（CSE）to simulate COPD， respectively，and the effect of overexpressed MTMR14 on COPD models in vitro and in vivo was investigated. Results MTMR14 expression was reduced in the lungs of COPD patients compared with that of the control group. MTMR14 overexpression inhibited CSE ⁃induced decrease in cell viability ，mitochondrial oxidative stress and inflammation，and improved mitochondrial function and mitophagy in vitro. Further validation was performed in COPD model mice. MTMR14 overexpression inhibited lung inflammatory cell infiltration，interstitial edema and congestion，and decreased serum IL ⁃6 and IL ⁃8 levels in COPD mice. In addition，MTMR14 overexpression im⁃ proved mitochondrial function and mitophagy to a certain extent and inhibited the excessive activation of mitophagy. Conclusions MTMR14 overexpression alleviates inflammation and emphysema in COPD，which in part depends on the regulation of mitochondrial function and mitophagy.