It is with great pleasure that I present to the readers of Gut this commentary accompanying the paper by McCarroll and colleagues¹ published in this issue of the journal (see page 79). The field of pancreatic stellate cell (PSC) research has grown exponentially in the past five years and major advancements have been made since their first identification as a pathophysiological entity at the end of the 1990s.^2,3 In those years, research on hepatic stellate cells (HSCs) and on their role in liver fibrogenesis had reached an elevated degree of sophistication. Therefore, the possibility of isolating stellate cells from rodent or human pancreas led to an almost automatic introduction of PSCs into a new research area: the cellular and molecular mechanisms of pancreatic fibrogenesis.

Fibrosis in the pancreas is consequent to necrosis/apoptosis, inflammation, or duct obstruction. The initial event that induces fibrogenesis in the pancreas is an injury that may involve the interstitial mesenchymal cells, duct cells, and/or acinar cells. Damage occurring in any of these tissue compartments is associated with cytokine triggered transformation of resident fibroblasts/pancreatic stellate cells into myofibroblasts and the subsequent production and deposition of extracellular matrix. The fibrogenic development depends on the site of injury and the involved tissue compartment. Deposition of excessive extracellular matrix is predominantly inter(peri)lobular (as in alcoholic chronic pancreatitis), periductal (as in hereditary pancreatitis), periductal and interlobular (as in autoimmune pancreatitis), or diffuse inter- and intralobular (as in obstructive chronic pancreatitis). In many ways, the development of pancreatic fibrosis recalls the different models of progressive scarring observed in liver tissue following chronic parenchymal damage or bile duct obstruction. Accordingly, it is likely that the two …