Autophagy is a highly conserved process by which cells can recycle organelles 
and proteins by degrading them in the lysosomes. Although autophagy is 
considered a dynamic system responsible for cellular renovation and homeostasis 
under physiological conditions, it is increasingly clear that autophagy is 
directly relevant to clinical disease. During disease progression, autophagy not 
only serves as a cellular protective mechanism but also can represent a harmful 
event under certain conditions. In addition, although autophagy can act as a 
nonselective bulk degradation process, recent research shows that autophagy can 
selectively degrade specific proteins, organelles, and invading bacteria, in 
processes termed "selective autophagy." Selective autophagy has drawn the 
attention of researchers because of its potential importance in clinical 
diseases. In this article, we outline the most recent studies implicating 
autophagy and selective autophagy in human lung diseases, including chronic 
obstructive pulmonary disease, pulmonary hypertension, idiopathic pulmonary 
fibrosis, and sepsis. We also discuss the relationship between autophagy and 
other molecular mechanisms related to disease progression, including programmed 
necrosis (necroptosis) and the inflammasome, an inflammatory signaling platform 
that regulates the secretion of IL-1β and IL-18. Finally, we examine the dual 
nature of autophagy and selective autophagy in the lung, which have both 
protective and injurious effects for human lung disease.