ReviewWorld journal of gastroenterology2006
Cholangiocyte anion exchange and biliary bicarbonate excretion.
Review in World journal of gastroenterology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
50 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Bile Acids Transporters of Enterohepatic Circulation for Targeted Drug Delivery.Molecules (Basel, Switzerland) · 2022Pooled it
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- Primary biliary cholangitis: A historical perspective from xanthomatous lesions to modern molecular biology.World journal of gastrointestinal pathophysiology · 2025Review
- Bile acid therapy for primary biliary cholangitis: Pathogenetic validation.World journal of experimental medicine · 2025Review
- Article
- New insights into the pathogenesis of primary biliary cholangitis asymptomatic stage.World journal of gastroenterology · 2023Review
- Active enterohepatic cycling is not required for the choleretic actions of 24-norUrsodeoxycholic acid in mice.JCI insight · 2023Article
- Genetics, pathobiology and therapeutic opportunities of polycystic liver disease.Nature reviews. Gastroenterology & hepatology · 2022Review
- Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics.Biomedicines · 2022Review
- Single-Cell, Single-Nucleus, and Spatial RNA Sequencing of the Human Liver Identifies Cholangiocyte and Mesenchymal Heterogeneity.Hepatology communications · 2022Article
- Design by Nature: Emerging Applications of Native Liver Extracellular Matrix for Cholangiocyte Organoid-Based Regenerative Medicine.Bioengineering (Basel, Switzerland) · 2022Review
- Functional, Diagnostic and Therapeutic Aspects of Bile.Clinical and experimental gastroenterology · 2022Article
- Polycystic Liver Disease: Pathophysiology, Diagnosis and Treatment.Hepatic medicine : evidence and research · 2022Review
- The Apical Sodium-Dependent Bile Acid Transporter in Cholangiocytes Is Not Required for the Generation of Bile Flow in Mice.Gastro hep advances · 2022Review
- The Genetics of Inherited Cholestatic Disorders in Neonates and Infants: Evolving Challenges.Genes · 2021Review
- Cell and Tissue Therapy for the Treatment of Chronic Liver Disease.Annual review of biomedical engineering · 2021Review
- The neglected biliary mucus and its phosphatidylcholine content: a putative player in pathogenesis of primary cholangitis-a narrative review article.Annals of translational medicine · 2021Review
- Bile duct reconstruction using scaffold-free tubular constructs created by Bio-3D printer.Regenerative therapy · 2021Article
- Review
- Inflammation in Primary and Metastatic Liver Tumorigenesis-Under the Influence of Alcohol and High-Fat Diets.Nutrients · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary canalicular bile undergoes a process of fluidization and alkalinization along the biliary tract that is influenced by several factors including hormones, innervation/neuropeptides, and biliary constituents. The excretion of bicarbonate at both the canaliculi and the bile ducts is an important contributor to the generation of the so-called bile-salt independent flow. Bicarbonate is secreted from hepatocytes and cholangiocytes through parallel mechanisms which involve chloride efflux through activation of Cl- channels, and further bicarbonate secretion via AE2/SLC4A2-mediated Cl-/HCO3- exchange. Glucagon and secretin are two relevant hormones which seem to act very similarly in their target cells (hepatocytes for the former and cholangiocytes for the latter). These hormones interact with their specific G protein-coupled receptors, causing increases in intracellular levels of cAMP and activation of cAMP-dependent Cl- and HCO3- secretory mechanisms. Both hepatocytes and cholangiocytes appear to have cAMP-responsive intracellular vesicles in which AE2/SLC4A2 colocalizes with cell specific Cl- channels (CFTR in cholangiocytes and not yet determined in hepatocytes) and aquaporins (AQP8 in hepatocytes and AQP1 in cholangiocytes). cAMP-induced coordinated trafficking of these vesicles to either canalicular or cholangiocyte lumenal membranes and further exocytosis results in increased osmotic forces and passive movement of water with net bicarbonate-rich hydrocholeresis.
Indexed as
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What OpenQuestion holds
Registered trials
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.