title: Molecular mechanisms of pancreatic injury.
abstract: OBJECTIVE
  Despite being a subject of much scientific scrutiny, the pathogenesis of acute pancreatitis is still not well understood. This article reviews recent advances in our understanding of acute pancreatitis.
  
  
  RESULTS
  Zymogen activation, observed within acini early during acute pancreatitis for a long time, was shown to be sufficient to induce acute pancreatitis. Another key early event, NFκB activation, has previously been shown to induce acute pancreatitis. The relationship between these two key early steps is beginning to be clarified. Mechanisms of zymogen activation - pathologic calcium signaling, pH changes, colocalization and autophagy, and of NFκB activation have been investigated intensively along with potential therapeutic targets both upstream and downstream of these key events. Additional key findings have been elucidation of the role of bioenergetics and the dual role of oxidative stress in acute pancreatitis, recognition of endoplasmic reticulum stress as an early step and the status of duct cells as important entities in pancreatic injury.
  
  
  CONCLUSIONS
  Current findings have provided further insight into the roles and mechanisms of zymogen activation and inflammatory pathways in pancreatic injury. Future studies, which will be of great importance in identifying therapeutic targets, are being undertaken to establish the relative contributions of these pathways during acute pancreatitis.
authors.affiliation: Division of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, Minnesota 55455, USA.
authors.forename: Raghuwansh P
authors.initials: RP
authors.lastname: Sah
authors.forename: Ashok
authors.initials: A
authors.lastname: Saluja
mesh_terms: D000818:Animals; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000502:physiology; D004734:Energy Metabolism; D004792:Enzyme Precursors / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D016328:NF-kappa B / Q000378:metabolism* / Q000502:physiology; D018384:Oxidative Stress; D010195:Pancreatitis / Q000209:etiology* / Q000378:metabolism* / Q000503:physiopathology; D015398:Signal Transduction
chemical_list: D004792:Enzyme Precursors; D016328:NF-kappa B