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