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Battle‐scarred pancreas: Role of alcohol and pancreatic stellate cells in pancreatic fibrosis
Author(s) -
Apte Minoti V,
Pirola Romano C,
Wilson Jeremy S
Publication year - 2006
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.2006.04587.x
Subject(s) - hepatic stellate cell , medicine , pancreatitis , pancreas , pancreatic injury , pancreatic disease , pancreatic cancer , fibrosis , cancer research , endocrinology , cancer
Pancreatic stellate cells (PSC) are now recognized as the key mediators of pancreatic fibrosis, a characteristic feature of chronic pancreatitis. The role of PSC in alcoholic pancreatic fibrosis has been examined in vivo (using pancreatic tissue from patients with alcohol‐induced chronic pancreatitis and from animal models of experimental pancreatitis) and in vitro (using PSC in culture). These studies indicate that PSC are activated early in the course of pancreatic injury and are the predominant source of collagen in the fibrotic pancreas. The factors responsible for mediating PSC activation during chronic alcohol exposure include ethanol, its metabolite acetaldehyde, oxidant stress and cytokines (released during episodes of alcohol‐induced pancreatic necroinflammation). Most recently, the intracellular signaling mechanisms regulating ethanol‐induced PSC activation have been identified and include the mitogen‐activated protein kinase (MAPK) pathway, phosphatidylinositol‐3‐kinase (PI3K) and protein kinase C (PKC), and the transcription factor activator protein‐1 (AP‐1).