Pathogenesis and progression of human pancreatic fibrosis

Fibrosis of the pancreas is one of the representative histopathological findings in cases of chronic pancreatitis. The pathogenesis and progression of pancreatic fibrosis are not yet fully understood. In this article, the pathogenesis, mechanism, and progression of pancreatic fibrosis are briefly reviewed based on our previous and most recent reports. Pancreatic fibrosis was classified into interlobular and intralobular types. In chronic alcoholic pancreatitis cases, fibrosis was mainly found in the interlobular, or perilobular, areas in a form of nodular pancreatitis. As for the mechanism of interlobular fibrosis, incomplete obstruction of the pancreatic duct and the appearance of the cells expressing alpha-smooth muscle actin, which is a marker for myofibroblasts, played an important role. In contrast, in intralobular fibrosis, alcohol intake was shown to have an effect in the initial stage of periacinar collagenization through the activation of myofibroblasts and severe damage to acinar cells. Progression of fibrosis occurred due to both duct obstruction and interlobular fibrosis admixed with myofibroblast proliferation. Therefore, myofibroblasts play an important role in both the mechanism and progression of pancreatic fibrosis.