ReviewWorld journal of gastroenterology2008
Aquaporins: their role in cholestatic liver disease.
Review in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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.
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
19 citing papers in PubMed, 41 citations in OpenAlex.
- Aquaporin membrane channels in the hepatobiliary tract: a model of complexity and clinical implications in health and disease.Internal and emergency medicine · 2026Review
- Expression and Immunolocalization of Aquaporins in the Buffalo Liver and Adipose Tissue.Journal of molecular histology · 2024Article
- Aquaporins in Biliary Function: Pathophysiological Implications and Therapeutic Targeting.International journal of molecular sciences · 2024Review
- Aquaporins: Potential Targets in Inflammatory Diseases.The Eurasian journal of medicine · 2023Article
- Review
- Aquaporin-8 ameliorates hepatic steatosis through farnesoid X receptor in obese mice.iScience · 2023Article
- Hepatic Aquaporin 10 Expression Is Downregulated by Activated NFκB Signaling in Human Obstructive Cholestasis.Gastro hep advances · 2023Article
- Non-Transport Functions of Aquaporins.Advances in experimental medicine and biology · 2023Article
- Review
- Hepatobiliary Thyroid Hormone Deficiency Impacts Bile Acid Hydrophilicity and Aquaporins in Cholestatic C57BL/6J Mice.International journal of molecular sciences · 2022Article
- The Pathological Mechanisms of Estrogen-Induced Cholestasis: Current Perspectives.Frontiers in pharmacology · 2021Review
- A structural preview of aquaporin 8 via homology modeling of seven vertebrate isoforms.BMC structural biology · 2018Article
- Function of aquaporins in sepsis: a systematic review.Cell & bioscience · 2018Review
- Aquaporins in Health and Disease: An Overview Focusing on the Gut of Different Species.International journal of molecular sciences · 2016Review
- A comprehensive analysis of aquaporin and secretory related gene expression in neonate and adult cholangiocytes.Gene expression patterns : GEP · 2014Article
- Pathogenic role of oxidative and nitrosative stress in primary biliary cirrhosis.World journal of gastroenterology · 2014Review
- Physiological and molecular biochemical mechanisms of bile formation.World journal of gastroenterology · 2013Review
- Bile formation and secretion.Comprehensive Physiology · 2013Review
- The molecular pathogenesis of cholestasis in sepsis.Frontiers in bioscience (Elite edition) · 2013Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review focuses on current knowledge on hepatocyte aquaporins (AQPs) and their significance in bile formation and cholestasis. Canalicular bile secretion results from a combined interaction of several solute transporters and AQP water channels that facilitate water flow in response to the osmotic gradients created. During choleresis, hepatocytes rapidly increase their canalicular membrane water permeability by modulating the abundance of AQP8. The question was raised as to whether the opposite process, i.e. a decreased canalicular AQP8 expression would contribute to the development of cholestasis. Studies in several experimental models of cholestasis, such as extrahepatic obstructive cholestasis, estrogen-induced cholestasis, and sepsis-induced cholestasis demonstrated that the protein expression of hepatocyte AQP8 was impaired. In addition, biophysical studies in canalicular plasma membranes revealed decreased water permeability associated with AQP8 protein downregulation. The combined alteration in hepatocyte solute transporters and AQP8 would hamper the efficient coupling of osmotic gradients and canalicular water flow. Thus cholestasis may result from a mutual occurrence of impaired solute transport and decreased water permeability.
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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.