Bidirectional regulation of pancreatic stellate cell-mediated pancreatic fibrosis by prostaglandin subtypes: mechanisms and therapeutic implications

Chronic pancreatitis (CP) is a recurrent inflammatory pancreatic disease characterized by progressive parenchymal damage. Currently, there are no effective clinical approaches to halt pancreatic fibrosis progression. As a core mediator involved in inflammation and fibrogenesis, prostaglandin (PG) participates in diverse inflammatory signaling cascades via the arachidonic acid metabolic pathway and further modulates pancreatic stellate cell (PSC) activation and extracellular matrix (ECM) deposition. This review systematically summarizes how distinct PG subtypes bind to corresponding receptors to regulate multiple signaling pathways and mediate PSC-related pancreatic fibrosis. It offers novel insights into developing targeted drugs against PG-related pathways and optimizing clinical treatment strategies for pancreatic fibrosis.