Autophagy is a crucial physiological process in cells and an important mechanism in the maintenance of cell homeostasis and regulation of cell survival. Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease of unknown etiology with a poor prognosis, characterized by alveolar epithelial cell damage and abnormal proliferation and activation of fibroblasts. IPF is accompanied by the excessive deposition of extracellular matrix(ECM), and its pathogenesis involves a complex interaction between cell types and signaling pathways. Defects in autophagy function have been shown to play a key role in the occurrence and development of IPF. This review aims to investigate the mechanism of autophagy in IPF and reveal its complexity and related signaling pathways.