Role of Bile Acids and Bile Salts in Acute Pancreatitis: From the Experimental to Clinical Studies
| Autor: | Julia Doller, Franziska Gisela Thiel, Frank Ulrich Weiss, Ali A. Aghdassi, M. Wiese, Anika Wilden, Laura L. De Freitas Chama, Markus M. Lerch, Robert Bolsmann, Matthias Sendler, Van Huy Tran, Jana Marielle Modenbach, Juliane Glaubitz, Quang Trung Tran |
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| Rok vydání: | 2020 |
| Předmět: |
acinar cells
BAs - bile acids Endocrinology Diabetes and Metabolism UDCA - ursodeoxycholic acid Pharmacology Endoplasmic Reticulum TUDCA - tauroursodeoxycholic acid PI3K - phosphatidylinositol 3-kinase RyR - ryanodine receptor 0302 clinical medicine Endocrinology CDCA - chenodeoxycholic acid NaT - sodium taurocholate Receptor Ca2 + IP3R - inositol triphosphate receptors Ryanodine receptor Chemistry SERCA - sarco/endoplasmic reticulum Ca2+ gallstone [Ca2+]i - intracellular calcium concentration Mitochondria Gpbar1 - G-protein–coupled bile acid receptor 1 medicine.anatomical_structure 030220 oncology & carcinogenesis 030211 gastroenterology & hepatology TCA - taurocholic acid Pancreas Signal Transduction Cell signaling acute pancreatitis FXR - farnesoid X receptor education TLCS - taurolithocholic acid-3-sulfate Reviews Bile Acids and Salts 03 medical and health sciences Necrosis Internal Medicine medicine Acinar cell AP - acute pancreatitis Animals Humans TCDC - taurochenodeoxycholic acid ATP - adenosine triphosphate bile acids Hepatology Endoplasmic reticulum Membrane Transport Proteins Inositol trisphosphate receptor NTCP - NaT cotransporting polypeptide Cytosol Disease Models Animal Pancreatitis Calcium IL - interleukin CCK - cholecystokinin |
| Zdroj: | Pancreas |
| ISSN: | 1536-4828 |
| Popis: | Acute pancreatitis (AP) is one of the most common gastroenterological disorders leading to hospitalization. It has long been debated whether biliary AP, about 30% to 50% of all cases, is induced by bile acids (BAs) when they reach the pancreas via reflux or via the systemic blood circulation. Besides their classical function in digestion, BAs have become an attractive research target because of their recently discovered property as signaling molecules. The underlying mechanisms of BAs have been investigated in various studies. Bile acids are internalized into acinar cells through specific G-protein–coupled BA receptor 1 and various transporters. They can further act via different receptors: the farnesoid X, ryanodine, and inositol triphosphate receptor. Bile acids induce a sustained Ca2+ influx from the endoplasmic reticulum and release of Ca2+ from acidic stores into the cytosol of acinar cells. The overload of intracellular Ca2+ results in mitochondrial depolarization and subsequent acinar cell necrosis. In addition, BAs have a biphasic effect on pancreatic ductal cells. A more detailed characterization of the mechanisms through which BAs contribute to the disease pathogenesis and severity will greatly improve our understanding of the underlying pathophysiology and may allow for the development of therapeutic and preventive strategies for gallstone-inducedAP. |
| Databáze: | OpenAIRE |
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