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Cell death in pancreatitis: Effects of alcohol
Author(s) -
Gukovskaya Anna S,
Mareninova Olga A,
Odinokova Irina V,
Sung KaiFeng,
Lugea Aurelia,
Fischer Lars,
Wang YanLing,
Gukovsky Ilya,
Pandol Stephen J
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.1440-1746.2006.04571.x
Subject(s) - pancreatitis , medicine , necrosis , acute pancreatitis , programmed cell death , apoptosis , acinar cell , pathogenesis , pathology , immunology , biology , biochemistry
Pancreatitis is a severe and frequently lethal disorder, a major cause of which is alcohol abuse. Parenchymal cell death is a major complication of pancreatitis. In experimental models of (non‐alcoholic) acute pancreatitis, acinar cells have been shown to die through both necrosis and apoptosis, the two principal pathways of cell death. The severity of experimental acute pancreatitis correlates directly with the extent of necrosis and inversely with apoptosis. Thus, understanding the regulation of apoptosis and necrosis, and whether it is possible to manipulate the pattern of death responses, is becoming exceedingly important in investigations of the pathogenesis and treatment of pancreatitis. The effects of alcohol on cell death responses of pancreatitis, and the mechanisms that may mediate these effects, are just starting to be explored. This paper reviews the signaling pathways mediating the balance between apoptosis and necrosis in acute pancreatitis, and alcohol’s effects on cell death responses in pancreatitis.