ArticleLiver international : official journal of the International Association for the Study of the Liver2012
Effect of bile duct ligation on bile acid composition in mouse serum and liver.
Article in Liver international : official journal of the International Association for the Study of the Liver, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
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Who cites it
95 citing papers in PubMed, 214 citations in OpenAlex.
- FDX1-mediated cuproptosis promotes cholestatic liver injury exacerbated by taurocholic acid-enhanced copper accumulation.Cell death discovery · 2026Article
- Serum total bile acids within the normal range are inversely associated with inflammatory indices and Gensini score in patients with premature coronary artery disease.Frontiers in immunology · 2026Article
- Comparative Evaluation of Analgesics in a Murine Bile Duct Ligation Model.Biomedicines · 2025Article
- Chenodeoxycholic acid modulates cholestatic niche through FXR/Myc/P-selectin axis in liver endothelial cells.Nature communications · 2025Article
- Inhibition of RAC1 activator DOCK2 ameliorates cholestatic liver injury via regulating macrophage polarisation and hepatic stellate cell activation.Biology direct · 2025Article
- Activation of S1PR2 on macrophages and the hepatocyte S1PR2/RhoA/ROCK1/MLC2 pathway in vanishing bile duct syndrome.PloS one · 2025Article
- Hepatic SIRT6 protects against cholestatic liver disease primarilyJournal of biomedical research · 2024Article
- Epithelial Na + Channel Activation after Bile Duct Ligation with Mineralocorticoid Receptor Blockade.Journal of the American Society of Nephrology : JASN · 2024Article
- Review
- BiliQML: a supervised machine-learning model to quantify biliary forms from digitized whole slide liver histopathological images.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Cholestasis-induced phenotypic transformation of neutrophils contributes to immune escape of colorectal cancer liver metastasis.Journal of biomedical science · 2024Article
- Multiscale X-ray phase-contrast CT unveils the evolution of bile infarct in obstructive biliary disease.Communications biology · 2024Article
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- Hepatic LGR4 aggravates cholestasis-induced liver injury in mice.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
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- Hepatic macrophage niche: a bridge between HBV-mediated metabolic changes with intrahepatic inflammation.Frontiers in immunology · 2024Review
- Apical bulkheads accumulate as adaptive response to impaired bile flow in liver disease.EMBO reports · 2023Article
- TNF-α/IL-1β-licensed hADSCs alleviate cholestatic liver injury and fibrosis in mice via COX-2/PGE2 pathway.Stem cell research & therapy · 2023Article
- Liver-restricted deletion of the biliary atresia candidate gene Pkd1l1 causes bile duct dysmorphogenesis and ciliopathy.Hepatology (Baltimore, Md.) · 2023Article
- Semi-Targeted Profiling of Bile Acids by High-Resolution Mass Spectrometry in a Rat Model of Drug-Induced Liver Injury.International journal of molecular sciences · 2023Article
35 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundCholestatic liver diseases can be caused by genetic defects, drug toxicities, hepatobiliary malignancies or obstruction of the biliary tract. Cholestasis leads to accumulation of bile acids (BAs) in hepatocytes. Direct toxicity of BAs is currently the most accepted hypothesis for cholestatic liver injury. However, information on which bile acids are actually accumulating during cholestasis is limited.
aimTo assess the BA composition in liver and serum after bile duct ligation (BDL) in male C57Bl/6 mice between 6 h and 14 days and evaluate toxicity of the most abundant BAs.
resultsBile acid concentrations increased in liver (27-fold) and serum (1400-fold) within 6 h after surgery and remained elevated up to 14 days. BAs in livers of BDL mice became more hydrophilic than sham controls, mainly because of increased 6β-hydroxylation and taurine conjugation. Among the eight unconjugated and 16 conjugated BAs identified in serum and liver, only taurocholic acid (TCA), β-muricholic acid (βMCA) and TβMCA were substantially elevated representing >95% of these BAs over the entire time course. Although glycochenodeoxycholic acid and other conjugated BAs increased in BDL animals, the changes were several orders of magnitude lower compared with TCA, βMCA and TβMCA. A mixture of these BAs did not cause apoptosis or necrosis, but induced inflammatory gene expression in cultured murine hepatocytes.
conclusionThe concentrations of cytotoxic BAs are insufficient to cause hepatocellular injury. In contrast, TCA, βMCA and TβMCA are able to induce pro-inflammatory mediators in hepatocytes. Thus, BAs act as inflammagens and not as cytotoxic mediators after BDL in mice.
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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.