Journal
GASTROENTEROLOGY
Volume 156, Issue 7, Pages 1951-+Publisher
W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.gastro.2018.11.081
Keywords
Trypsinogen; Pancreatitis; Genetics; Inflammation; Cell Death
Categories
Funding
- PePPP Center of Excellence [MV ESF/14-BM-A55-0045/16, ESF MV V-630-S-150-2012/132/133, DFG-CRC 1321.-P14, DFG SE 2702/2-1]
- National Institutes of Health [R01 DK058088, R01 DK117809]
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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.
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