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In the current study by Ishiwatari et al, a novel antifibrotic therapy has been shown to revert pancreatic fibrosis induced by dibutyltin dichloride and cerulein in rats.1 The authors have previously used this approach to resolve fibrosis in various models of liver cirrhosis in rats.2 The compound used in both studies is an siRNA against collagen-specific chaperone protein gp46 (HSP47 in humans), encapsulated in vitamin A-coupled liposomes (VA-lip-siRNAgp46). This approach exploits the pivotal roles of stellate cells in fibrogenesis as well as in the uptake and storage of vitamin A in the target organs.
Quiescent pancreatic stellate cells (PSC) belong to the stellate cell system consisting of retinoid-storing cells in various organs.3 Upon pancreatic injury or during carcinogenesis, PSC are activated by cytokines, growth factors, reactive oxygen species as well as mechanical factors such as increased intraductal pressure or by a stiff extracellular matrix (ECM). Upon activation, PSC transdifferentiate into a myofibroblast-like phenotype and produce ECM proteins. PSC activation is associated with loss of cytoplasmic vitamin A (retinol) stores.
Activated PSC are responsible for producing the desmoplastic stroma of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. Replacement of the normal parenchyma by fibrosis leads to exocrine and endocrine insufficiency in chronic pancreatitis. …
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