Commentaries
Pancreatitis: the neglected duct
1 Department of Pharmacology, Yonsei University College of Medicine, Seoul, Korea
2 Department of Physiology, University of Texas Southwestern Medical Center, Dallas, Texas, USA
Correspondence to:
Dr Shmuel Muallem, Department of Physiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-9040, USA; Schmuel.muallem@utsouthwestern.edu
| The first 150 words of the full text of this article appear below. |
Acute and chronic pancreatitis are multifactorial diseases that involve inflammation of the pancreas, generation of toxic mediators and mistargeting of digestive enzymes that eventually result in destruction of the parenchyma.1 Because acinar cells contain the harmful mistargeted digestive enzymes and the extensive damage occurs in acinar cells in all forms and models of pancreatitis, research into the triggers and causes of pancreatitis have been focused on acinar cells.1 It is now well established that aberrant Ca2+ signalling leading to a sustained and prolonged increase in free cytoplasmic Ca2+ concentration ([Ca2+]i) is the nodal point in pancreatitis that perturbs many functions of acinar cells, leading to their destruction.
While undoubtedly destruction of acinar cells is the terminal step in pancreatitis, the duct is likely to play a crucial role in protecting the pancreas, and when this protection is compromised pancreatitis ensues. The central function of the pancreatic duct is
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Gut 2008 57: 1102-1112.[Abstract] [Full Text] [PDF]
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