ReviewGene expression2019
Inflammation and Cell Death During Cholestasis: The Evolving Role of Bile Acids.
Review in Gene expression, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 59 citations in OpenAlex.
- Immunometabolic crosstalk in gallstone disease: driving roles of bacterial infection, NETs and MMP activation.Molecular biology reports · 2026Review
- Slippery dopamine-fluoropolymer hybrid surface for improving biliary stent longevity.Bioactive materials · 2026Article
- Deficiency of ZFP36L1 and ZFP36L2 impairs liver homeostasis and initiates cholestatic liver injury.Hepatology communications · 2026Article
- Hepatoprotective Effect of Cynarin on Alpha-Naphthyl Isothiocyanate-Induced Cholestatic Liver Injury: Associated Modulation of TXNIP/NLRP3 and HMGB1/NF-κB Signaling Cascades.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Cell-based approaches for the mechanistic understanding of drug-induced cholestatic liver injury.Archives of toxicology · 2025Review
- Intraduodenal fecal microbiota transplantation ameliorates gut atrophy and cholestasis in a novel parenteral nutrition piglet model.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- Insights into the pathogenesis of gestational and hepatic diseases: the impact of ferroptosis.Frontiers in cell and developmental biology · 2024Review
- Uncovering a Novel Functional Interaction Between Adult Hepatic Progenitor Cells, Inflammation and EGFR Signaling During Bile Acids-Induced Injury.International journal of biological sciences · 2024Article
- Comparative Study on the Effects of Four Plant Protein Sources on the Liver and Intestinal Health of Largemouth Bass,Aquaculture nutrition · 2024Article
- Human Hepatocellular response in Cholestatic Liver Diseases.Organogenesis · 2023Article
- Article
- Cirrhotic Cardiomyopathy Following Bile Duct Ligation in Rats-A Matter of Time?International journal of molecular sciences · 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
- Uncovering key molecules and immune landscape in cholestatic liver injury: implications for pathogenesis and drug therapy.Frontiers in pharmacology · 2023Article
- Review
- Protocols of Investigation of Neonatal Cholestasis-A Critical Appraisal.Healthcare (Basel, Switzerland) · 2022Review
- The liver in sepsis: molecular mechanism of liver failure and their potential for clinical translation.Molecular medicine (Cambridge, Mass.) · 2022Review
- Melatonin prevents oxidative stress, inflammatory activity, and DNA damage in cirrhotic rats.World journal of gastroenterology · 2022Article
- Case Report: Dramatic Cholestasis Responsive to Steroids in a Newborn Homozygous for H63D HFE Variant.Frontiers in pediatrics · 2022Article
- Hepatoprotective Effects of Glycyrrhetinic Acid on Lithocholic Acid-Induced Cholestatic Liver Injury Through Choleretic and Anti-Inflammatory Mechanisms.Frontiers in pharmacology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cholestasis results in blockage of bile flow whether the point of obstruction occurs extrahepatically or intrahepatically. Bile acids are a primary constituent of bile, and thus one of the primary outcomes is acute retention of bile acids in hepatocytes. Bile acids are normally secreted into the biliary tracts and then released into the small bowel before recirculating back to the liver. Retention of bile acids has long been hypothesized to be a primary cause of the associated liver injury that occurs during acute or chronic cholestasis. Despite this, a surge of papers in the last decade have reported a primary role for inflammation in the pathophysiology of cholestatic liver injury. Furthermore, it has increasingly been recognized that both the constituency of individual bile acids that make up the greater pool, as well as their conjugation status, is intimately involved in their toxicity, and this varies between species. Finally, the role of bile acids in drug-induced cholestatic liver injury remains an area of increasing interest. The purpose of this review is to critically evaluate current proposed mechanisms of cholestatic liver injury, with a focus on the evolving role of bile acids in cell death and inflammation.
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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.