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The role of Ca2+ in the pathophysiology of pancreatitis

Gerasimenko, Julia Vladimirovna ORCID:, Gerasimenko, Oleg Vsevolodovich ORCID: and Petersen, Ole Holger ORCID: 2014. The role of Ca2+ in the pathophysiology of pancreatitis. The Journal of Physiology 592 (2) , pp. 269-280. 10.1113/jphysiol.2013.261784

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Acute pancreatitis is a human disease in which the pancreatic pro-enzymes, packaged into the zymogen granules of the acinar cells, become activated and cause auto-digestion. 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 excessive release of Ca2+ from intracellular stores, followed by excessive entry of Ca2+ from the interstitial fluid. However, Ca2+ release and subsequent entry are also precisely the processes that control physiological secretion of the digestive enzymes in response to stimulation via the vagal nerve or the hormone cholecystokinin. The spatial and temporal Ca2+ 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 blockade of Ca2+ release-activated Ca2+ currents in pancreatic acinar cells offers remarkable protection against Ca2+ overload, intracellular protease activation and necrosis evoked by a combination of alcohol and fatty acids, which is a major trigger of acute pancreatitis.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
Systems Immunity Research Institute (SIURI)
Subjects: Q Science > QH Natural history > QH301 Biology
R Medicine > R Medicine (General)
Uncontrolled Keywords: Calcium (Ca2+) ATPase; Calcium (Ca2+) transport; Pancreatic acinar cell
Publisher: The Physiological Society
ISSN: 0022-3751
Funders: MRC
Date of First Compliant Deposit: 30 March 2016
Last Modified: 15 May 2023 16:59

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