HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (28) Citing Articles via Google Scholar Google Scholar Articles by Bhatia, M. Search for Related Content PubMed PubMed Citation Articles by Bhatia, M.

INVITED REVIEWS

Apoptosis versus necrosis in acute pancreatitis

Department of Pharmacology, National University of Singapore, Singapore 117597

Submitted 13 July 2003 ; accepted in final form 8 September 2003

Acute pancreatitis is a disease of variable severity in which some patients experience mild, self-limited attacks, whereas others manifest a severe, highly morbid, and frequently lethal attack. The events that regulate the severity of acute pancreatitis are, for the most part, unknown. It is generally believed that the earliest events in acute pancreatitis occur within acinar cells and result in acinar cell injury. Other processes, such as recruitment of inflammatory cells and generation of inflammatory mediators, are believed to occur subsequent to acinar cell injury, and these "downstream" events are believed to influence the severity of the disease. Several recently reported studies, however, have suggested that the acinar cell response to injury may, itself, be an important determinant of disease severity. In these studies, mild acute pancreatitis was found to be associated with extensive apoptotic acinar cell death, whereas severe acute pancreatitis was found to involve extensive acinar cell necrosis but very little acinar cell apoptosis. These observations led to the hypothesis that apoptosis could be a favorable response to acinar cells and that interventions that favor induction of apoptotic, as opposed to necrotic, acinar cell death might reduce the severity of an attack of acute pancreatitis. Indeed, in an experimental setting, the induction of pancreatic acinar cell apoptosis protects mice against acute pancreatitis. Little is known about the mechanism of apoptosis in the pancreatic acinar cell, although some early attempts have been made in that direction. Also, clinical relevance of these experimental studies remains to be investigated.

acute pancreatitis; pancreatic acinar cells

This article has been cited by other articles:

				A. S. Kowalik, C. L. Johnson, S. A. Chadi, J. Y. Weston, E. N. Fazio, and C. L. Pin Mice lacking the transcription factor Mist1 exhibit an altered stress response and increased sensitivity to caerulein-induced pancreatitis Am J Physiol Gastrointest Liver Physiol, April 1, 2007; 292(4): G1123 - G1132. [Abstract] [Full Text] [PDF]

				Y. Cao, S. Adhikari, A. D. Ang, P. K. Moore, and M. Bhatia Mechanism of induction of pancreatic acinar cell apoptosis by hydrogen sulfide Am J Physiol Cell Physiol, September 1, 2006; 291(3): C503 - C510. [Abstract] [Full Text] [PDF]

				Y. Cao, S. Adhikari, A. D. Ang, M. V. Clement, M. Wallig, and M. Bhatia Crambene induces pancreatic acinar cell apoptosis via the activation of mitochondrial pathway Am J Physiol Gastrointest Liver Physiol, July 1, 2006; 291(1): G95 - G101. [Abstract] [Full Text] [PDF]

				F. Fortunato, X. Deng, L. K. Gates, C. J. McClain, D. Bimmler, R. Graf, and D. C. Whitcomb Pancreatic response to endotoxin after chronic alcohol exposure: switch from apoptosis to necrosis? Am J Physiol Gastrointest Liver Physiol, February 1, 2006; 290(2): G232 - G241. [Abstract] [Full Text] [PDF]