4.8 Review

Inflammation, Autophagy, and Obesity: Common Features in the Pathogenesis of Pancreatitis and Pancreatic Cancer

Journal

GASTROENTEROLOGY
Volume 144, Issue 6, Pages 1199-+

Publisher

W B SAUNDERS CO-ELSEVIER INC
DOI: 10.1053/j.gastro.2013.02.007

Keywords

Pancreatic Acinar Cell; Cytokines; Neutrophil; Pancreatic Ductal Adenocarcinoma; K-Ras

Funding

  1. Department of Veterans Affairs
  2. National Institutes of Health [DK59936]
  3. Pancreatic Cancer Research Lustgarten Foundation grant [RFP-B-007]
  4. Erwin Schrodinger Fellowship of the Austrian Science Fund [J 3233]
  5. [P01 CA163200]
  6. [AA19730]
  7. [AI043477]
  8. [CA163798]
  9. [P50 AA011999]
  10. [R03CA167120]

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Inflammation and autophagy are cellular defense mechanisms. When these processes are deregulated (deficient or overactivated) they produce pathologic effects, such as oxidative stress, metabolic impairments, and cell death. Unresolved inflammation and disrupted regulation of autophagy are common features of pancreatitis and pancreatic cancer. Furthermore, obesity, a risk factor for pancreatitis and pancreatic cancer, promotes inflammation and inhibits or deregulates autophagy, creating an environment that facilitates the induction and progression of pancreatic diseases. However, little is known about how inflammation, autophagy, and obesity interact to promote exocrine pancreatic disorders. We review the roles of inflammation and autophagy, and their deregulation by obesity, in pancreatic diseases. We discuss the connections among disordered pathways and important areas for future research.

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