Fibrogenesis in the pancreas after acinar cell injury.
Fibrosis within the pancreas is a key feature of chronic pancreatitis and pancreatic cancer. It has now been well demonstrated that following injury to acinar cells, pancreatic stellate cell activation, migration and proliferation is the key mediator of this process. Many cytokines and growth factors have been studied, particularly TGF-beta, which appears to be the major stimulus to fibrinogenesis. There is current interest in the mechanisms of phenotypic change between the active and quiescent forms, apoptosis and the signalling pathways that may be involved. The pancreatic stellate cell is likely to play an important role in maintaining the normal extracellular matrix; we speculate that the dysregulation of this process is an important factor in chronic pancreatitis.
Patel
M
M
Southampton University Hospitals NHS Trust, Southampton, UK.
Fine
D R
DR
D017209:Apoptosis / Q000502:physiology; D051017:Apoptosis Regulatory Proteins; D002908:Chronic Disease; D005355:Fibrosis; D006801:Humans; D008562:Membrane Glycoproteins / Q000378:metabolism; D045726:Metalloproteases / Q000502:physiology; D010179:Pancreas / Q000166:cytology* / Q000378:metabolism / Q000473:pathology*; D010195:Pancreatitis / Q000503:physiopathology; D053221:TNF-Related Apoptosis-Inducing Ligand; D016212:Transforming Growth Factor beta / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D051017:Apoptosis Regulatory Proteins; D008562:Membrane Glycoproteins; D053221:TNF-Related Apoptosis-Inducing Ligand; C505653:TNFSF10 protein, human; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D045726:Metalloproteases