Pancreatic stellate cells (PaSCs) are classified as myofibroblast-like cells that are located in exocrine regions of the pancreas. PaSCs are mediated by paracrine and autocrine stimuli and share similarities with the hepatic stellate cell. Pancreatic stellate cell activation and expression of matrix molecules constitute the complex process that induces pancreatic fibrosis. Synthesis, deposition, maturation and remodelling of the fibrous connective tissue can be protective, however when persistent it impedes regular pancreatic function. Structure PaSCs are located within the peri-acinar spaces of the pancreas and extrude long cytoplasmic processes that surround the base of the acinus. PaSCs compose 4% of the total cell mass in the gland Stellate cells derive their name from their star shape and are located in other organs such as the kidney and lungs. The cells are located in periductal and perivascular regions of the pancreas and contain vitamin A lipid droplets in their cytoplasm. PaSCs engage in disease pathogenesis by transforming from a quiescent state into an activated state, which is also known as a “myofibroblastic” state. PaSCs express the intermediate filament proteins desmin and glial fibrillary acidic protein. The expression of a diverse range of intermediate filament proteins enables the PaSC to harbour contractile abilities. Cellular extensions also enable the cells to sense their environment. Following inflammation or injury to the pancreas, quiescent PaSCs are activated to myofibroblast like cells, which expresses α- smooth muscle actin. Several morphological changes take place including nuclear enlargement and increased growth of the endoplasmic reticulum network. The activated PaSCs then grow in number, migrate and secrete extracellular matrix components such as type I collagen, chemokines and cytokines. Function Quiescent PaSCs produce metalloproteinases such as MMP-2, MMP-9, and MMP-13 and their inhibitors, which assist in the turnover of the extracellular matrix (ECM). As a result of regulating ECM turnover, PaSCs are involved in the maintenance of the modelling of normal tissue. MMP-2 secreted by PaSCs, however, contributes to the development of pancreatic cancer. Fibrosis is a prominent feature of chronic pancreatitis and of the desmoplastic reaction linked with pancreatic cancer. While the pathogenesis of fibrosis remains elusive, the activation of stellate cells contribute to pancreatic fibrosis. Numerous soluble factors regulate PaSC activation, specifically IL-1, IL-6, TNF-α, TGF-B1 and activin 1. The potential sources of these activating factors include platelets, macrophages, pancreatic acinar cells and endothelial cells in inflamed pancreas. PaSCs, individually, are also capable of synthesising cytokines such as TGF-β1,