Acute pancreatitis (AP) is a prevalent gastrointestinal condition characterized by an inflammatory response in the pancreas, with a global prevalence of 4.9-73.4 per 100,000 individuals. As the disease advances, its severity and prognosis fluctuate. Mechanisms of programmed cell death (PCD) include apoptosis, ferroptosis, and autophagy; understanding their interactions is crucial for maintaining cellular homeostasis. Each pathway represents a distinct PCD process, and current studies emphasize the complex interrelationships and reciprocal effects among them. Therefore, investigating these interactions is essential for understanding how cells determine their fate and how these mechanisms contribute to various illnesses. Increasing evidence indicates that PCD significantly contributes to the development of AP, and drugs targeting various forms of PCD constitute a possible treatment approach. Consequently, understanding the function and mechanism of PCD in AP enhances our understanding of its pathophysiological mechanisms and offers substantial benefits for the management of AP. The review's importance lies in examining the interactions among ferroptosis, apoptosis, and autophagy, with critical implications for the development of therapeutic approaches, especially in conditions characterized by dysregulated cell death. By analyzing the biochemical interactions among these pathways, scientists may identify novel drug targets and develop strategies to regulate cell fate successfully. This review examines the interplay and crosstalk among apoptosis, autophagy, and ferroptosis signaling pathways in the regulation of AP development.
