title: Drinking and driving pancreatitis: links between endoplasmic reticulum stress and autophagy.
abstract: Alcohol abuse is the leading etiologic factor of pancreatitis, although many heavy drinkers do not develop pancreatic damage. Alcohol promotes pancreatitis through a combination of remote (e.g., increased gut permeability to bacterial products such as lipopolysaccharide) and more proximal effects (e.g., altered pancreatic cholinergic inputs), including oxidative damage at the level of the pancreatic acinar cell. Recent evidence indicates that alcohol exposure to rodents disturbs proteostasis in the exocrine pancreas, an effect counterbalanced by homeostatic processes that include both the unfolded protein response (UPR) and autophagy. A corollary to this notion is that pancreatitis results when adaptive responses are insufficiently robust to alleviate the cellular stress caused by alcohol.
authors: Southern California Research Center for ALPD & Cirrhosis, VA Greater Los Angeles Healthcare System and University of California, Los Angeles, Los Angeles, CA, USA. alugea@ucla.edu
authors: Aurelia
authors: A
authors: Lugea
authors: Richard T
authors: RT
authors: Waldron
authors: Samuel W
authors: SW
authors: French
authors: Stephen J
authors: SJ
authors: Pandol
mesh_terms: D000428:Alcohol Drinking / Q000009:adverse effects*; D000818:Animals; D001343:Autophagy; D004268:DNA-Binding Proteins / Q000172:deficiency / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000473:pathology*; D051379:Mice; D008954:Models, Biological; D010179:Pancreas / Q000378:metabolism / Q000473:pathology; D010195:Pancreatitis / Q000473:pathology*; D000071701:Regulatory Factor X Transcription Factors; D013312:Stress, Physiological; D014157:Transcription Factors / Q000172:deficiency / Q000378:metabolism
chemical_list: D004268:DNA-Binding Proteins; D000071701:Regulatory Factor X Transcription Factors; D014157:Transcription Factors