Related Experiment Video
Updated: Jul 8, 2026

A Simple and Rapid Method for Simultaneous Isolation of Primary Islets and Primary Pancreatic Acinar Cells from Mice
Published on: January 9, 2026
Mitochondrial injury in pancreatitis
R Mukherjee1, D N Criddle, A Gukovskaya
1Division of Surgery and Oncology, University of Liverpool, Royal Liverpool University Hospital, Daulby Street, Liverpool, United Kingdom.
Abstract:
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.
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