The main results of this study can be summarized as follows: (1) the significant lower expression of MTMR14 in the lung of COPD patients compared with controls indicates the possibility of MTMR14 as a novel regulatory mechanism; (2) in vitro, MTMR14 inhibited CSE-induced inflammation and apoptosis in bronchial epithelial cells, and further mechanism studies revealed that the biological regulation of MTMR14 was, to a certain extent, dependent on the regulation of mitochondrial function and mitophagy; and (3) in vivo, MTMR14 reduced inflammation and improved emphysema in COPD model mice. This evidence concerns the gene MTMR14 and pulmonary emphysema.