ArticleThe American journal of pathology2016
Bile Acid Signaling Is Involved in the Neurological Decline in a Murine Model of Acute Liver Failure.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 104 citations in OpenAlex.
- Infusion of donor feces affects the gut-brain axis in humans with metabolic syndrome.Molecular metabolism · 2020Trial
- Gut microbiota-driven metabolites modulate the development of stress-related mental disorders.Translational psychiatry · 2026Review
- Gut microbiome and bile acid metabolism in liver disease: Mechanisms, clinical implications, and therapeutic opportunities.Pharmacological reviews · 2026Review
- The Collaborative Collapse: Bile Acid Dysmetabolism as a Central Pathogenic Driver in Canine and Feline Multi-Systemic Disorders-From Mechanisms to Precision Therapeutics.Veterinary sciences · 2026Review
- Microbiota and Alzheimer's disease: mechanistic insights from a multi-organ perspective.Translational neurodegeneration · 2026Review
- Proinflammatory state and metabolic dysregulation linking delayed feeding progression to extrauterine restricted head growth in extremely preterm infants.BMC medicine · 2025Article
- Gut-Brain Axis and Bile Acid Signaling: Linking Microbial Metabolism to Brain Function and Metabolic Regulation.International journal of molecular sciences · 2025Review
- Targeting gut microbiota in liver disease: A pharmacological approach for hepatic encephalopathy and beyond.World journal of gastrointestinal pharmacology and therapeutics · 2025Review
- Dietary cholesterol impairs cognition via gut microbiota-derived deoxycholic acid in obese mice.Gut microbes · 2025Article
- Beyond the gut: decoding the gut-immune-brain axis in health and disease.Cellular & molecular immunology · 2025Review
- Risk factors for hepatic encephalopathy after transjugular intrahepatic portosystemic shunt in cirrhotic patients: A comprehensive minireview.World journal of hepatology · 2025Review
- Dysregulation of bile acid signal transduction causes neurological dysfunction in cirrhosis rats.World journal of hepatology · 2025Article
- Linking Brain and Immune Transcriptomes to Gut-Derived Metabolites in Hepatic Encephalopathy: An Explorative Integrative Multi-Omics Approach.Hepatic medicine : evidence and research · 2025Article
- Effects of cholestasis and hyperammonemia on dendritic spine density and turnover in rat hippocampal neurons.Scientific reports · 2024Article
- Underneath the Gut-Brain Axis in IBD-Evidence of the Non-Obvious.International journal of molecular sciences · 2024Review
- Emerging Roles of Bile Acids and TGR5 in the Central Nervous System: Molecular Functions and Therapeutic Implications.International journal of molecular sciences · 2024Review
- Gut Microbiota Metabolite Messengers in Brain Function and Pathology at a View of Cell Type-Based Receptor and Enzyme Reaction.Biomolecules & therapeutics · 2024Review
- Elderly mice with history of acetaminophen intoxication display worsened cognitive impairment and persistent elevation of astrocyte and microglia burden.Scientific reports · 2024Article
- Gut Microbiota and Its Metabolites: The Emerging Bridge Between Coronary Artery Disease and Anxiety and Depression?Aging and disease · 2024Review
- Article
13 more citing papers are in PubMed but not listed here.
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
Hepatic encephalopathy is a serious neurological complication of liver failure. Serum bile acids are elevated after liver damage and may disrupt the blood-brain barrier and enter the brain. Our aim was to assess the role of serum bile acids in the neurological complications after acute liver failure. C57Bl/6 or cytochrome p450 7A1 knockout (Cyp7A1(-/-)) mice were fed a control, cholestyramine-containing, or bile acid-containing diet before azoxymethane (AOM)-induced acute liver failure. In parallel, mice were given an intracerebroventricular infusion of farnesoid X receptor (FXR) Vivo-morpholino before AOM injection. Liver damage, neurological decline, and molecular analyses of bile acid signaling were performed. Total bile acid levels were increased in the cortex of AOM-treated mice. Reducing serum bile acids via cholestyramine feeding or using Cyp7A1(-/-) mice reduced bile acid levels and delayed AOM-induced neurological decline, whereas cholic acid or deoxycholic acid feeding worsened AOM-induced neurological decline. The expression of bile acid signaling machinery apical sodium-dependent bile acid transporter, FXR, and small heterodimer partner increased in the frontal cortex, and blocking FXR signaling delayed AOM-induced neurological decline. In conclusion, circulating bile acids may play a pathological role during hepatic encephalopathy, although precisely how they dysregulate normal brain function is unknown. Strategies to minimize serum bile acid concentrations may reduce the severity of neurological complications associated with liver failure.
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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.