Autophagy is a process of lysosomal self-degradation that helps to maintain the homeostatic balance between the synthesis, degradation and recycling of cellular proteins and organelles. Autophagy does not simply function as the machinery for supplying amino acids in response to energy demands, it is an adaptive pathway of cytoprotection against cellular stressors, including starvation, reactive oxygen species (ROS), endoplasmic reticulum (ER) stress and microbial infection. Accordingly, autophagy is considered to be the mediator of a variety of cellular processes and cell fates, including cell survival and death, cellular senescence and immune responses. Due to the organ-specific role of gas exchange, various cell types within the lungs are serially exposed to a diverse array of cellular stressors, and growing evidence has revealed the crucial involvement of autophagy in the pathogenic processes underlying pulmonary diseases. We herein review recent findings regarding the role of autophagy in cellular processes and cell fates and summarize the role that autophagy appears to play in the pathogenesis of pulmonary diseases.