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532545 
Journal Article 
Review 
Molecular mechanisms of pancreatitis: Current opinion 
Vonlaufen, A; Wilson, JS; Apte, MV 
2008 
Yes 
Journal of Gastroenterology and Hepatology
ISSN: 0815-9319
EISSN: 1440-1746 
23 
9 
1339-1348 
English 
18853993 
WOS:000258595900007 
Pancreatitis (necroinflammation of the pancreas) has both acute and chronic manifestations. Gallstones are the major cause of acute pancreatitis, whereas alcohol is associated with acute as well as chronic forms of the disease. Cases of true idiopathic pancreatitis are steadily diminishing as more genetic causes of the disease are discovered. The pathogenesis of acute pancreatitis has been extensively investigated over the past four decades; the general current consensus is that the injury is initiated within pancreatic acinar cells subsequent to premature intracellular activation of digestive enzymes. Repeated attacks of acute pancreatitis have the potential to evolve into chronic disease characterized by fibrosis and loss of pancreatic function. Our knowledge of the process of scarring has advanced considerably with the isolation and study of pancreatic stellate cells, now established as the key cells in pancreatic fibrogenesis. The present review summarizes recent developments in the field particularly with respect to the progress made in unraveling the molecular mechanisms of acute and chronic pancreatic injury secondary to gallstones, alcohol and genetic factors. It is anticipated that continued research in the area will lead to the identification and characterization of molecular pathways that may be therapeutically targeted to prevent/inhibit the initiation and progression of the disease. 
acetaldehyde; acinar cell; acute pancreatitis; alcohol; alcohol; metabolism; chronic pancreatitis; fatty acid ethyl ester; genetic; polymorphism; stellate cell; acid ethyl-esters; alcoholic chronic-pancreatitis; cationic trypsinogen; gene; idiopathic chronic-pancreatitis; tropical calcific pancreatitis; serine-protease inhibitor; cystic-fibrosis gene; hereditary; pancreatitis; biliary-tract; acinar-cells