ArticleGastroenterology2012
Alterations in lipid metabolism mediate inflammation, fibrosis, and proliferation in a mouse model of chronic cholestatic liver injury.
Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers.
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
71 citing papers in PubMed, 159 citations in OpenAlex.
- Biomarkers of NAFLD progression: a lipidomics approach to an epidemic.Journal of lipid research · 2015Trial
- Scratching the Surface: Lipidomic Profiling of the Stratum Corneum in the Search for Pruritogens in Cholestatic Liver Diseases.Journal of personalized medicine · 2026Review
- The conjugation-resistant bile acid norUDCA cures liver fibrosis but impairs systemic energy metabolism.Molecular metabolism · 2026Article
- Metabolic heterogeneity, networks, and biomarkers of drug-induced liver injury.Journal of pharmaceutical analysis · 2026Article
- iPLA2β-null mice exposed to natural pathogens exhibit hepatocellular fibrotic injury with male-biased alteration of glycerolipid metabolism.Frontiers in immunology · 2026Article
- The history and future of bile acid therapies.Journal of hepatology · 2025Article
- Clinical characteristics of dyslipidemia in patients with primary biliary cholangitis: a single-center experience in China.Clinical rheumatology · 2025Article
- Benefits and challenges to therapeutic targeting of bile acid circulation in cholestatic liver disease.Hepatology (Baltimore, Md.) · 2025Review
- Sildenafil blunts cholestasis-associated cholemic nephropathy in a rat model of bile duct ligation.Clinical and experimental hepatology · 2025Article
- Primary sclerosing cholangitis.Nature reviews. Disease primers · 2025Review
- Targeting the ceramidase ACER3 attenuates cholestasis in mice by mitigating bile acid overload via unsaturated ceramide-mediated LXRβ signaling transduction.Nature communications · 2025Article
- TBK1-associated adapters TANK and AZI2 protect mice against TNF-induced cell death and severe autoinflammatory diseases.Nature communications · 2024Article
- Serum metabonomics reveal the effectiveness of human placental mesenchymal stem cell therapy for primary sclerosing cholangitis.Stem cell research & therapy · 2024Article
- WTAP boosts lipid oxidation and induces diabetic cardiac fibrosis by enhancing AR methylation.iScience · 2023Article
- Treatment of primary sclerosing cholangitis combined with inflammatory bowel disease.Intestinal research · 2023Review
- [Response to Primary Biliary Cholangitis Treatment: Influencing Factors and the Role in Prognosis Prediction].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2023Article
- Colitis ameliorates cholestatic liver disease via suppression of bile acid synthesis.Nature communications · 2023Article
- Active enterohepatic cycling is not required for the choleretic actions of 24-norUrsodeoxycholic acid in mice.JCI insight · 2023Article
- Ameliorative Effect ofInternational journal of molecular sciences · 2023Article
- Schizandrin C regulates lipid metabolism and inflammation in liver fibrosis by NF-κB and p38/ERK MAPK signaling pathways.Frontiers in pharmacology · 2023Article
11 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsThe liver controls central processes of lipid and bile acid homeostasis. We aimed to investigate whether alterations in lipid metabolism contribute to the pathogenesis of chronic cholestatic liver disease in mice.
methodsWe used microarray and metabolic profiling analyses to identify alterations in systemic and hepatic lipid metabolism in mice with disruption of the gene ATP-binding cassette sub-family B member 4 (Abcb4(-/-) mice), a model of inflammation-induced cholestatic liver injury, fibrosis, and cancer.
resultsAlterations in Abcb4(-/-) mice, compared with wild-type mice, included deregulation of genes that control lipid synthesis, storage, and oxidation; decreased serum levels of cholesterol and phospholipids; and reduced hepatic long-chain fatty acyl-CoAs (LCA-CoA). Feeding Abcb4(-/-) mice the side chain-modified bile acid 24-norursodeoxycholic acid (norUDCA) reversed their liver injury and fibrosis, increased serum levels of lipids, lowered phospholipase and triglyceride hydrolase activities, and restored hepatic LCA-CoA and triglyceride levels. Additional genetic and nutritional studies indicated that lipid metabolism contributed to chronic cholestatic liver injury; crossing peroxisome proliferator-activated receptor (PPAR)-α-deficient mice with Abcb4(-/-) mice (to create double knockouts) or placing Abcb4(-/-) mice on a high-fat diet protected against liver injury, with features similar to those involved in the response to norUDCA. Placing pregnant Abcb4(-/-) mice on high-fat diets prevented liver injury in their offspring. However, fenofibrate, an activator of PPARα, aggravated liver injury in Abcb4(-/-) mice.
conclusionsAlterations in lipid metabolism contribute to the pathogenesis and progression of cholestatic liver disease in mice.
Indexed as
Identifiers
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.