The early phase of both acute and chronic pancreatitis can be characterized by disrupt level and function of the cystic fibrosis transmembrane conductance regulator (CFTR) Cl(-) channel, decreased bicarbonate secretion, intraductal acidosis, decrease of fluid secretion and elevation of mucoprotein levels. It is almost needless to say that these intrapancreatic changes are very similar to the pathophysiological changes observed in cystic fibrosis. The aim of this mini review is to describe the development of the above mentioned pathological observations in details, moreover highlight some future therapeutic opportunities in pancreatitis.
Disproportionate reduction in tryptic response to endogenous compared with exogenous stimulation in chronic pancreatitis
Observations on 205 confirmed cases of acute pancreatitis, recurring pancreatitis, and chronic pancreatitis
The cystic fibrosis transmembrane conductance regulator activates aquaporin 3 in airway epithelial cells.
Hereditary pancreatitis caused by a novel PRSS1 mutation (Arg-122 --> Cys) that alters autoactivation and autodegradation of cationic trypsinogen
Reducing extracellular pH sensitizes the acinar cell to secretagogue-induced pancreatitis responses in rats
CFTR expression but not Cl- transport is involved in the stimulatory effect of bile acids on apical Cl-/HCO3- exchange activity in human pancreatic duct cells
Corticosteroids correct aberrant CFTR localization in the duct and regenerate acinar cells in autoimmune pancreatitis
Non-conjugated chenodeoxycholate induces severe mitochondrial damage and inhibits bicarbonate transport in pancreatic duct cells
Trypsin reduces pancreatic ductal bicarbonate secretion by inhibiting CFTR Cl⁻ channels and luminal anion exchangers
Ethanol and its non-oxidative metabolites profoundly inhibit CFTR function in pancreatic epithelial cells which is prevented by ATP supplementation
Association of bone morphogenetic protein 6 with exocrine gland dysfunction in patients with Sjögren's syndrome and in mice
Cigarette smoke induces systemic defects in cystic fibrosis transmembrane conductance regulator function
Fatty acid ethyl ester synthase inhibition ameliorates ethanol-induced Ca2+-dependent mitochondrial dysfunction and acute pancreatitis
Effect of magnesium supplementation and depletion on the onset and course of acute experimental pancreatitis
Lactate reduces liver and pancreatic injury in Toll-like receptor- and inflammasome-mediated inflammation via GPR81-mediated suppression of innate immunity
Glucose-induced electrical activities and insulin secretion in pancreatic islet β-cells are modulated by CFTR
Mechanisms of CFTR functional variants that impair regulated bicarbonate permeation and increase risk for pancreatitis but not for cystic fibrosis
Mnk1 is a novel acinar cell-specific kinase required for exocrine pancreatic secretion and response to pancreatitis in mice
Alcohol disrupts levels and function of the cystic fibrosis transmembrane conductance regulator to promote development of pancreatitis.
Acute pancreatitis. Evidence-based practice guidelines, prepared by the Hungarian Pancreatic Study Group
Overexpression of PD2 leads to increased tumorigenicity and metastasis in pancreatic ductal adenocarcinoma
Poly(ADP-Ribose) Polymerase 1 Promotes Inflammation and Fibrosis in a Mouse Model of Chronic Pancreatitis.
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