November 12, 2014
Notes: Gornik, Ivan
Gubarev Vrdoljak, Nina
Pancreatology. 2013 May-Jun;13(3):196-200. doi: 10.1016/j.pan.2013.03.008. Epub 2013 Mar 14.
Author Address: University Hospital Centre Zagreb, Department of Medicine, Kispaticeva 12, Zagreb, Croatia. email@example.com
Reference Type: Journal Article
Record Number: 5292Author: Gukovsky, I., Li, N., Todoric, J., Gukovskaya, A. and Karin, M.
Title: Inflammation, autophagy, and obesity: common features in the pathogenesis of pancreatitis and pancreatic cancer
Pages: 1199-209 e4
Short Title: Inflammation, autophagy, and obesity: common features in the pathogenesis of pancreatitis and pancreatic cancer
Alternate Journal: Gastroenterology
ISSN: 1528-0012 (Electronic)
Accession Number: 23622129
Abstract: 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.