The role of Ca2+ in the pathophysiology of pancreatitis
Open accessAbstract
Acute pancreatitis is a human disease in which the pancreatic pro‐enzymes, packaged into the zymogen granules of acinar cells, become activated and cause autodigestion. The main causes of pancreatitis are alcohol abuse and biliary disease. A considerable body of evidence indicates that the primary event initiating the disease process is the excessive release of Ca 2+ from intracellular stores, followed by excessive entry of Ca 2+ from the interstitial fluid. However, Ca 2+ release and subsequent entry are also precisely the processes that control the physiological secretion of digestive enzymes in response to stimulation via the vagal nerve or the hormone cholecystokinin. The spatial and temporal Ca 2+ signal patterns in physiology and pathology, as well as the contributions from different organelles in the different situations, are therefore critical issues. There has recently been significant progress in our understanding of both physiological stimulus–secretion coupling and the pathophysiology of acute pancreatitis. Very recently, a promising potential therapeutic development has occurred with the demonstration that the blockade of Ca 2+ release‐activated Ca 2+ currents in pancreatic acinar cells offers remarkable protection against Ca 2+ overload, intracellular protease activation and necrosis evoked by a combination of alcohol and fatty acids, which is a major trigger of acute pancreatitis.
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In acute pancreatitis a similar cascade of intra- and extracellular reactions leads to fatty acid ethyl esters-induced increase of the Ca2+ release which results in massive necrosis of pancreatic acinar cells and acute inflammation.
“In acute pancreatitis a similar cascade of intra‐ and extracellular reactions leads to fatty acid ethyl esters (FAEE)‐induced increase of the Ca2+ release which results in massive necrosis of pancreatic acinar cells 307 and acute inflammation.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [307]
This process is mediated by sustained elevation of the cytosolic Ca2+ levels and results ultimately in releasing pancreatic enzymes into the interstitium and in chronic inflammation.
“This process is mediated by sustained elevation of the cytosolic Ca2+ levels 307 and results ultimately in releasing pancreatic enzymes into the interstitium and in chronic inflammation 299.”
From The relationship between different dimensions of alcohol use and the burden of disease—an update (2017) · cites this paper as [307]
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The relationship between different dimensions of alcohol use and the burden of disease—an update
Rehm, J., Gmel, G. E., Gmel, G., Hasan, O. S. M., Imtiaz, S., Popova, S., Probst, C., Roerecke, M., Room, R., Samokhvalov, A. V., et al. (2017) · Addiction · doi:10.1111/add.13757 · Cited by 1,204 · see citing works
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The heparin-binding proteome in normal pancreas and murine experimental acute pancreatitis
Nunes, Q. M., Su, D., Brownridge, P. J., Simpson, D. M., Sun, C., Li, Y., Bui, T. P., Zhang, X., Huang, W., Rigden, D. J., et al. (2019) · PLOS ONE · doi:10.1371/journal.pone.0217633 · Cited by 42 · see citing works
- Authors
- Gerasimenko, J. V., Gerasimenko, O. V., & Petersen, O. H.
- Affiliations
- Cardiff University (GB)
- Corresponding author
- Petersen, Ole H.
- Venue
- The Journal of Physiology
- Publisher
- Wiley
- Published
- 2013-09-02
- Volume
- 592
- Issue
- 2
- Pages
- 269-280
- ISSN
- 0022-3751 (ISSN-L)
- 1469-7793
- PMC
- PMC3922492
- OpenAlex
- W2155710425
- Cited by
- 143
- References
- 86
- Citations by year
- 2026: 9 · 2025: 8 · 2024: 16 · 2023: 8 · 2022: 3 · 2021: 13 · 2020: 15 · 2019: 15 · 2018: 12 · 2017: 14 · 2016: 13 · 2015: 9 · 2014: 8
- FWCI
- 1.89
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- The Journal of Physiology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- ORCA Online Research @Cardiff (Cardiff University) (acceptedVersion)
- Topics
- Health Sciences › Medicine › Surgery › Pancreatitis Pathology and Treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Physiology › Calcium signaling and nucleotide metabolism
- Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
- Keywords
- acute pancreatitis, calcium signaling, intracellular calcium release, calcium overload, pancreatic acinar cells, zymogen granules, calcium release-activated calcium current, stimulus-secretion coupling, cholecystokinin, vagus nerve, alcoholic pancreatitis, fatty acids, necrosis
- MeSH terms
- Animals, Calcium, Calcium Channel Blockers, Humans, Pancreatitis, Calcium Channels, Calcium Signaling, Secretory Vesicles
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