New insights into regulatory cell death and acute pancreatitis

Acute pancreatitis (AP) may be associated with both local and systemic complications. Although it is usually self-limiting, up to 20% of patients develop severe acute pancreatitis (SAP), which leads to systemic inflammatory response syndrome (SIRS) and multiorgan dysfunction and failure affecting the lung, kidney, liver and heart. Patients who survive the condition frequently develop devastating long-term consequences such as diabetes mellitus, exocrine pancreatic insufficiency, chronic pancreatitis (CP) and poor quality of life. A lack of specific targeted treatments is the main reason for high mortality and morbidity, indicating that more research on the pathogenesis of AP is needed. In the past decade, substantial advancements have been made in our understanding of the pathophysiological mechanisms of AP, including mechanisms of calcium-mediated acinar cell injury and death, the cytoprotective role of the unfolded protein response (UPR) and autophagy in preventing sustained endoplasmic reticulum stress (ERs); however, the mechanism of parenchymal cell death is relatively poorly understood. This paper reviews the research progress of the regulatory cell death (RCD) mode in the pathogenesis of AP, providing some new insights and regulatory targets for the pathogenesis and treatment of AP, facilitating better targeted drug development.