Mitochondrial injury in pancreatitis

Summary Pancreatitis is an increasingly common disease that carries a significant mortality and which lacks specific therapy. Pathological calcium signalling is an important contributor to the initiating cell injury, caused by or acting through mitochondrial inhibition. A principal effect of disorde...

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Bibliographic Details
Published in:Cell calcium (Edinburgh) 2008-07, Vol.44 (1), p.14-23
Main Authors: Mukherjee, R, Criddle, D.N, Gukvoskaya, A, Pandol, S, Petersen, O.H, Sutton, R
Format: Article
Language:English
Subjects:
Advanced Basic Science
Animals
Antioxidants - therapeutic use
Calcium Signaling - physiology
Caspases - metabolism
Cell Death - physiology
Humans
Mitochondria - genetics
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Membrane Transport Proteins - physiology
Oxidative Stress - physiology
Pancreas - enzymology
Pancreas - pathology
Pancreas - physiopathology
Pancreas - ultrastructure
Pancreatitis - etiology
Pancreatitis - metabolism
Pancreatitis - physiopathology
Pancreatitis - therapy
Reactive Oxygen Species - adverse effects
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Summary:Summary Pancreatitis is an increasingly common disease that carries a significant mortality and which lacks specific therapy. Pathological calcium signalling is an important contributor to the initiating cell injury, caused by or acting through mitochondrial inhibition. A principal effect of disordered cell signalling and impaired mitochondrial function is cell death, either by apoptosis that is primarily protective, or by necrosis that is deleterious, both locally and systemically. Mitochondrial calcium overload is particularly important in necrotic injury, which may include damage mediated by the mitochondrial permeability transition pore. The role of reactive oxygen species remains controversial. Present understanding of the part played by disordered pancreatic acinar calcium signalling and mitochondrial inhibition offers several new potential therapeutic targets.
ISSN:0143-4160
1532-1991
DOI:10.1016/j.ceca.2007.11.013