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• W148301145 endingPage "16146" @default.
• W148301145 startingPage "16146" @default.
• W148301145 abstract "Pancreatitis is an increasingly common and sometimes severe disease that lacks a specific therapy. The pathogenesis of pancreatitis is still not well understood. Calcium (Ca(2+)) is a versatile carrier of signals regulating many aspects of cellular activity and plays a central role in controlling digestive enzyme secretion in pancreatic acinar cells. Ca(2+) overload is a key early event and is crucial in the pathogenesis of many diseases. In pancreatic acinar cells, pathological Ca(2+) signaling (stimulated by bile, alcohol metabolites and other causes) is a key contributor to the initiation of cell injury due to prolonged and global Ca(2+) elevation that results in trypsin activation, vacuolization and necrosis, all of which are crucial in the development of pancreatitis. Increased release of Ca(2+) from stores in the intracellular endoplasmic reticulum and/or increased Ca(2+) entry through the plasma membrane are causes of such cell damage. Failed mitochondrial adenosine triphosphate (ATP) production reduces re-uptake and extrusion of Ca(2+) by the sarco/endoplasmic reticulum Ca(2+)-activated ATPase and plasma membrane Ca(2+)-ATPase pumps, which contribute to Ca(2+) overload. Current findings have provided further insight into the roles and mechanisms of abnormal pancreatic acinar Ca(2+) signals in pancreatitis. The lack of available specific treatments is therefore an objective of ongoing research. Research is currently underway to establish the mechanisms and interactions of Ca(2+) signals in the pathogenesis of pancreatitis." @default.
• W148301145 created "2016-06-24" @default.
• W148301145 creator A5018064299 @default.
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• W148301145 creator A5038916155 @default.
• W148301145 creator A5057209439 @default.
• W148301145 date "2014-01-01" @default.
• W148301145 modified "2023-10-16" @default.
• W148301145 title "Calcium signaling of pancreatic acinar cells in the pathogenesis of pancreatitis" @default.
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• W148301145 doi "https://doi.org/10.3748/wjg.v20.i43.16146" @default.
• W148301145 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4239501" @default.
• W148301145 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25473167" @default.
• W148301145 hasPublicationYear "2014" @default.
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