Pathobiology of acute pancreatitis: focus on intracellular calcium and calmodulin

Petersen, Ole Holger ORCID: https://orcid.org/0000-0002-6998-0380, Gerasimenko, Oleg Vsevolodovich ORCID: https://orcid.org/0000-0003-2573-8258 and Gerasimenko, Julia Vladimirovna ORCID: https://orcid.org/0000-0002-2262-2543 2011. Pathobiology of acute pancreatitis: focus on intracellular calcium and calmodulin. F1000 Medicine Reports (3) , 15. 10.3410/M3-15

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Abstract

The exocrine pancreas synthesizes all the enzymes needed for intestinal breakdown of proteins, fats, and carbohydrates in our diet. Unfortunately, the proteases needed for the digestion of the meat we eat can, if inappropriately activated inside the acinar cells, also digest the pancreas itself as well as the surrounding tissues, which is what happens in the sometimes fatal human disease acute pancreatitis. The disease is currently untreatable, but significant progress has recently been made in understanding the fundamental processes initiating the pathological changes underlying pancreatic autodigestion. It is now clear that intracellular trypsin activation—a crucial step in pathogenesis—is due to excessive release of Ca2+ from intracellular stores, principally via two types of inositol trisphosphate receptor. The unexpected recent discovery of an intrinsic protective mechanism caused by intracellular calmodulin and, specifically, the finding that this protective effect can be boosted by a membrane-permeable Ca2+-like peptide are promising.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences Systems Immunity Research Institute (SIURI)
Subjects:	Q Science > Q Science (General)
Publisher:	Faculty of 1000
ISSN:	1757-5931
Date of First Compliant Deposit:	30 March 2016
Last Modified:	13 May 2023 12:34
URI:	https://orca.cardiff.ac.uk/id/eprint/25763

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