Regeneration and Repair of the Exocrine Pancreas

Pancreatitis is caused by inflammatory injury to the exocrine pancreas, from which both humans and animal models appear to recover via regeneration of digestive enzyme-producing acinar cells. This regenerative process involves transient phases of inflammation, metaplasia, and redifferentiation, driv...

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Bibliographic Details
Published in:Annual review of physiology 2015-01, Vol.77 (1), p.229-249
Main Authors: Murtaugh, L. Charles, Keefe, Matthew D
Format: Article
Language:English
Subjects:
acinar cell
Acinar Cells - cytology
Acinar Cells - physiology
Animals
caerulein
Cell Differentiation - physiology
Cells
cerulein
differentiation
Disease Models, Animal
Exocrine glands
Humans
inflammation
metaplasia
Pancreas, Exocrine - cytology
Pancreas, Exocrine - physiology
Pancreatic cancer
Pancreatic Neoplasms - pathology
Pancreatic Neoplasms - physiopathology
pancreatitis
Pancreatitis - pathology
Pancreatitis - physiopathology
Regeneration - physiology
Signal transduction
Signal Transduction - physiology
Tissue engineering
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Summary:Pancreatitis is caused by inflammatory injury to the exocrine pancreas, from which both humans and animal models appear to recover via regeneration of digestive enzyme-producing acinar cells. This regenerative process involves transient phases of inflammation, metaplasia, and redifferentiation, driven by cell-cell interactions between acinar cells, leukocytes, and resident fibroblasts. The NFκB signaling pathway is a critical determinant of pancreatic inflammation and metaplasia, whereas a number of developmental signals and transcription factors are devoted to promoting acinar redifferentiation after injury. Imbalances between these proinflammatory and prodifferentiation pathways contribute to chronic pancreatitis, characterized by persistent inflammation, fibrosis, and acinar dedifferentiation. Loss of acinar cell differentiation also drives pancreatic cancer initiation, providing a mechanistic link between pancreatitis and cancer risk. Unraveling the molecular bases of exocrine regeneration may identify new therapeutic targets for treatment and prevention of both of these deadly diseases.
ISSN:0066-4278
1545-1585
DOI:10.1146/annurev-physiol-021014-071727