Aims: The present study is to investigate the expression of microRNA (miR)-130a in chronic obstructive pulmonary disease (COPD) tissues, as well as its function and potential mechanism. Methods: A total of 43 patients with COPD who received lobectomy due to pulmonary bulla at our hospital between August 2012 and January 2015 were included in the present study. Tissues at the foci and those more than 5 cm away from the foci were included into COPD and normal control groups, respectively. Quantitative real-time polymerase chain reaction was used to measure the expression of miR-130a. After transfection with miR-130a mimics, Cell-Counting Kit 8 assay and flow cytometry, were used to study the proliferation, cell cycle and apoptosis of primary human pulmonary alveolar epithelial cells (HPAEpiCs). Western blotting was used to measure the expression of ATG16L and electron microscopy was used to study the autophagy of HPAEpiCs. Dual luciferase reporter assay was carried out to identify the direct binding between ATG16L and miR-130a. Results: Expression of miR-130a was elevated in COPD tissues. Overexpression of miR-130a inhibited the proliferation of HPAEpiCs possibly by controlling the transition between G1 and S phases. Overexpression of miR-130a facilitated the apoptosis of HPAEpiCs and aggravated damages in the lungs. miR-130a regulated the expression of ATG16L that exerted its biological effect by facilitating the apoptosis of HPAEpiCs. miR-130a reduced autophagy activity of HPAEpiCs by targeting ATG16L. Conclusions: The present study demonstrates that the expression of miR-130a in COPD tissues is elevated, and miR-130a facilitates the occurrence and development of COPD by inhibiting autophagy and promoting apoptosis of HPAEpiCs.