Document Detail


Molecular mechanisms of pancreatic injury.
MedLine Citation:
PMID:  21844752     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
PURPOSE OF REVIEW: Despite being a subject of much scientific scrutiny, the pathogenesis of acute pancreatitis is still not well understood. This article reviews recent advances in our understanding of acute pancreatitis.
RECENT FINDINGS: Zymogen activation, observed within acini early during acute pancreatitis for a long time, was shown to be sufficient to induce acute pancreatitis. Another key early event, NFκB activation, has previously been shown to induce acute pancreatitis. The relationship between these two key early steps is beginning to be clarified. Mechanisms of zymogen activation - pathologic calcium signaling, pH changes, colocalization and autophagy, and of NFκB activation have been investigated intensively along with potential therapeutic targets both upstream and downstream of these key events. Additional key findings have been elucidation of the role of bioenergetics and the dual role of oxidative stress in acute pancreatitis, recognition of endoplasmic reticulum stress as an early step and the status of duct cells as important entities in pancreatic injury.
SUMMARY: Current findings have provided further insight into the roles and mechanisms of zymogen activation and inflammatory pathways in pancreatic injury. Future studies, which will be of great importance in identifying therapeutic targets, are being undertaken to establish the relative contributions of these pathways during acute pancreatitis.
Authors:
Raghuwansh P Sah; Ashok Saluja
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Current opinion in gastroenterology     Volume:  27     ISSN:  1531-7056     ISO Abbreviation:  Curr. Opin. Gastroenterol.     Publication Date:  2011 Sep 
Date Detail:
Created Date:  2011-08-16     Completed Date:  2012-01-13     Revised Date:  2012-04-26    
Medline Journal Info:
Nlm Unique ID:  8506887     Medline TA:  Curr Opin Gastroenterol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  444-51     Citation Subset:  IM    
Affiliation:
Division of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, Minnesota 55455, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Endoplasmic Reticulum / metabolism,  physiology
Energy Metabolism
Enzyme Precursors / metabolism*,  physiology
Humans
NF-kappa B / metabolism*,  physiology
Oxidative Stress
Pancreatitis / etiology*,  metabolism*,  physiopathology
Signal Transduction
Grant Support
ID/Acronym/Agency:
R01 DK058694/DK/NIDDK NIH HHS; R01 DK058694/DK/NIDDK NIH HHS; R01 DK092145-02/DK/NIDDK NIH HHS; R01 DK093047/DK/NIDDK NIH HHS; R01 DK093047-02/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Precursors; 0/NF-kappa B

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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