title: Early events in acute pancreatitis.
abstract: Considerable progress in the understanding of the pathogenesis of acute pancreatitis is based on the conclusive finding that the initiation of the disease occurs within the acinar cell. Two lines of evidence have contributed to the progress in understanding the disease process: (1) the identification of patients with a hereditary form of pancreatitis as carriers of germline-mutations in the genes for cationic trypsinogen and the pancreatic secretory trypsin inhibitor and (2) the use of various transgenic and knock-out mouse strains in experimental models of acute pancreatitis. On the other hand, these studies have delivered several unexpected results that appear to be incompatible with long-standing dogmas and paradigms of pancreatic research. Further progress in knowledge will result if the well-characterized enzymatic properties of human enzymes that are involved in the initial activation cascade can be investigated under in vivo conditions in transgenic animals or in permanent acinar cell lines. Such studies will permit the development of effective strategies for the prevention and treatment of this disease.
authors.affiliation: Division of Experimental Surgery, Department of Surgery, Otto-von-Guericke-Universität, Magdeburg, Leipziger Strasse, 44 D-39120 Magdeburg, Germany. walter.halangk@medizin.uni-magdeburg.de
authors.forename: Walter
authors.initials: W
authors.lastname: Halangk
authors.forename: Markus M
authors.initials: MM
authors.lastname: Lerch
mesh_terms: D000208:Acute Disease; D000818:Animals; D020013:Calcium Signaling / Q000502:physiology; D002401:Cathepsin B / Q000378:metabolism*; D006801:Humans; D046790:Pancreas, Exocrine / Q000201:enzymology*; D010195:Pancreatitis / Q000378:metabolism* / Q000503:physiopathology*; D014357:Trypsin / Q000378:metabolism*
chemical_list: D014357:Trypsin; D002401:Cathepsin B