Genetics, Cell Biology, and Pathophysiology of Pancreatitis.

Abstract

Since the discovery of the first trypsinogen mutation in families with hereditary pancreatitis, pancreatic genetics has made rapid progress. The identification of mutations in genes involved in the digestive protease-antiprotease pathway has lent additional support to the notion that pancreatitis is a disease of autodigestion. Clinical and experimental observations have provided compelling evidence that premature intrapancreatic activation of digestive proteases is critical in pancreatitis onset. However, disease course and severity are mostly governed by inflammatory cells that drive local and systemic immune responses. In this article, we review the genetics, cell biology, and immunology of pancreatitis with a focus on protease activation pathways and other early events.

• Authors: Julia Mayerle, Matthias Sendler, Eszter Hegyi, Georg Beyer, Markus M Lerch, Miklós Sahin-Tóth
• Journal: Gastroenterology (Gastroenterology) Vol. 156 Issue 7 Pg. 1951-1968.e1 (05 2019) ISSN: 1528-0012 [Electronic] United States
• PMID: 30660731 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't, Review)
• Copyright: Copyright © 2019 AGA Institute. Published by Elsevier Inc. All rights reserved.

Chemical References

• Inflammation Mediators
• Peptide Hydrolases

Topics

• Animals
• Apoptosis
• Enzyme Activation
• Genetic Predisposition to Disease
• Humans
• Inflammation Mediators (metabolism)
• Mutation
• Necrosis
• Pancreas (enzymology, immunology, pathology, physiopathology)
• Pancreatitis (enzymology, genetics, pathology, physiopathology)
• Peptide Hydrolases (genetics, metabolism)
• Phenotype
• Prognosis
• Protein Folding
• Risk Factors
• Signal Transduction