Autophagy is a major catabolic process in which cells remove damaged, defective or useless organelles, long-lived proteins and lipids from the cytoplasm, and recycle their components to meet the nutritional and energy needs of biological metabolism. Acute pancreatitis (AP) is a common critical disease, and its prevalence continues to rise in recent years. Studies have demonstrated that autophagy plays an important role in the pathogenesis of AP, it can cause trypsinogen activation and accumulation of large vacuoles in the pancreatic acinar cells, and induce the release of proinflammatory mediators, and thereby cause inflammatory cell infiltration of the pancreas and systemic inflammatory response. Here, the authors address the molecular mechanism of autophagy and the mechanism of autophagy in the occurrence and development of AP.