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- W2938782689 endingPage "470" @default.
- W2938782689 startingPage "459" @default.
- W2938782689 abstract "Acute pancreatitis (AP) is a potentially lethal inflammatory disease that lacks specific therapy. Damaged pancreatic acinar cells are believed to be the site of AP initiation. The primary function of these cells is the synthesis, storage, and export of digestive enzymes. Beginning in the endoplasmic reticulum and ending with secretion of proteins stored in zymogen granules, distinct pancreatic organelles use ATP produced by mitochondria to move and modify nascent proteins through sequential vesicular compartments. Compartment-specific accessory proteins concentrate cargo and promote vesicular budding, targeting, and fusion. The autophagy-lysosomal-endosomal pathways maintain acinar cell homeostasis by removing damaged/dysfunctional organelles and recycling cell constituents for substrate and energy. Here, we discuss studies in experimental and genetic AP models, primarily from our groups, which show that acinar cell injury is mediated by distinct mechanisms of organelle dysfunction involved in protein synthesis and trafficking, secretion, energy generation, and autophagy. These early AP events (often first manifest by abnormal cytosolic Ca2+ signaling) in the acinar cell trigger the inflammatory and cell death responses of pancreatitis. Manifestations of acinar cell organelle disorders are also prominent in human pancreatitis. Our findings suggest that targeting specific mediators of organelle dysfunction could reduce disease severity." @default.
- W2938782689 created "2019-04-25" @default.
- W2938782689 creator A5001192190 @default.
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- W2938782689 creator A5061294594 @default.
- W2938782689 creator A5082812084 @default.
- W2938782689 creator A5082828872 @default.
- W2938782689 date "2019-04-01" @default.
- W2938782689 modified "2023-10-16" @default.
- W2938782689 title "Recent Insights Into the Pathogenic Mechanism of Pancreatitis" @default.
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