ArticleGastroenterology2003
Loss of inositol 1,4,5-trisphosphate receptors from bile duct epithelia is a common event in cholestasis.
Article in Gastroenterology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
58 citing papers in PubMed, 124 citations in OpenAlex.
- Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.Clinical science (London, England : 1979) · 2025Review
- Analysis and Regulatory Mechanisms of Platelet-Related Genes in Patients with Ischemic Stroke.Cellular and molecular neurobiology · 2024Article
- Type 3 IP3 receptor: Its structure, functions, and related disease implications.Channels (Austin, Tex.) · 2023Review
- New insights into the pathogenesis of primary biliary cholangitis asymptomatic stage.World journal of gastroenterology · 2023Review
- The Hepatic Mitochondrial Alterations Exacerbate Meta-Inflammation in Autism Spectrum Disorders.Antioxidants (Basel, Switzerland) · 2022Article
- Roles of Non-Coding RNAs in Primary Biliary Cholangitis.Frontiers in molecular biosciences · 2022Review
- Involvement of oxidative species in cyclosporine-mediated cholestasis.Frontiers in pharmacology · 2022Review
- Inositol 1,4,5-trisphosphate receptor type 3 (ITPR3) is overexpressed in cholangiocarcinoma and its expression correlates with S100 calcium-binding protein A4 (S100A4).Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Article
- Neutrophils interact with cholangiocytes to cause cholestatic changes in alcoholic hepatitis.Gut · 2021Article
- Therapeutic Opportunities of GPBAR1 in Cholestatic Diseases.Frontiers in pharmacology · 2021Review
- Ethanol Disrupts Hormone-Induced Calcium Signaling in Liver.Function (Oxford, England) · 2021Article
- Inositol 1,4,5-trisphosphate receptor type 3 plays a protective role in hepatocytes during hepatic ischemia-reperfusion injury.Cell calcium · 2020Article
- Type 3 Inositol 1,4,5-Trisphosphate Receptor Is Increased and Enhances Malignant Properties in Cholangiocarcinoma.Hepatology (Baltimore, Md.) · 2020Article
- Review
- Characterization of NCS1-InsP3R1 interaction and its functional significance.The Journal of biological chemistry · 2019Article
- Inositol 1,4,5-trisphosphate receptor in the liver: Expression and function.World journal of gastroenterology · 2019Review
- Effects of Endotoxin on Type 3 Inositol 1,4,5-Trisphosphate Receptor in Human Cholangiocytes.Hepatology (Baltimore, Md.) · 2019Article
- Calcium Signaling in Cholangiocytes: Methods, Mechanisms, and Effects.International journal of molecular sciences · 2018Review
- Bi-allelic CCDC47 Variants Cause a Disorder Characterized by Woolly Hair, Liver Dysfunction, Dysmorphic Features, and Global Developmental Delay.American journal of human genetics · 2018Article
- NCS-1 is a regulator of calcium signaling in health and disease.Biochimica et biophysica acta. Molecular cell research · 2018Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND AND
aimsCholestasis is one of the principal manifestations of liver disease and often results from disorders involving bile duct epithelia rather than hepatocytes. A range of disorders affects biliary epithelia, and no unifying pathophysiologic event in these cells has been identified as the cause of cholestasis. Here we examined the role of the inositol 1,4,5-trisphosphate receptor (InsP3R)/Ca(2+) release channel in Ca(2+) signaling and ductular secretion in animal models of cholestasis and in patients with cholestatic disorders.
methodsThe expression and distribution of the InsP3R and related proteins were examined in rat cholangiocytes before and after bile duct ligation or treatment with endotoxin. Ca(2+) signaling was examined in isolated bile ducts from these animals, whereas ductular bicarbonate secretion was examined in isolated perfused livers. Confocal immunofluorescence was used to examine cholangiocyte InsP3R expression in human liver biopsy specimens.
resultsExpression of the InsP3R was selectively lost from biliary epithelia after bile duct ligation or endotoxin treatment. As a result, Ca(2+) signaling and Ca(2+)-mediated bicarbonate secretion were lost as well, although other components of the Ca(2+) signaling pathway and adenosine 3',5'-cyclic monophosphate (cAMP)-mediated bicarbonate secretion both were preserved. Examination of human liver biopsy specimens showed that InsP3Rs also were lost from bile duct epithelia in a range of human cholestatic disorders, although InsP3R expression was intact in noncholestatic liver disease.
conclusionsInsP3-mediated Ca(2+) signaling in bile duct epithelia appears to be important for normal bile secretion in the liver, and loss of InsP3Rs may be a final common pathway for cholestasis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.