Evidence map›Paper›PMID 35068796›Full record

ReviewJournal of clinical and experimental hepatology

A Current Understanding of Bile Acids in Chronic Liver Disease.

Naba Farooqui, Anshuman Elhence, Shalimar

Open access · greenAbstract readReview
In one paragraph

Review in Journal of clinical and experimental hepatology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.7field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

48 citing papers in PubMed, 79 citations in OpenAlex.

  1. Review
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  16. Serum Metabolite Profile in Progressive Versus Nonprogressive Alcohol-Related Liver Disease: A Cross-Sectional Metabolomics Study.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  17. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 3 institutions in 2 countries.

Naba FarooquiDivision of Nephrology and Hypertension, Mayo Clinic, Rochester, MN, USA.
Anshuman ElhenceDepartment of Gastroenterology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, India.
ShalimarDepartment of Gastroenterology and Human Nutrition, All India Institute of Medical Sciences, New Delhi, India.
All India Institute of Medical Sciences · INMayo Clinic · USSanjay Gandhi Post Graduate Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic liver disease (CLD) is one of the leading causes of disability-adjusted life years in many countries. A recent understanding of nuclear bile acid receptor pathways has increased focus on the impact of crosstalk between the gut, bile acids, and liver on liver pathology. While conventionally used in cholestatic disorders and to dissolve gallstones, the discovery of bile acids' influence on the gut microbiome and human metabolism offers a unique potential for their utility in early and advanced liver diseases because of diverse etiologies. Based on these findings, preclinical studies using bile acid-based molecules have shown encouraging results at addressing liver inflammation and fibrosis. Emerging data also suggest that bile acid profiles change distinctively across various causes of liver disease. We summarize the current knowledge and evidence related to bile acids in health and disease and discuss culminated and ongoing therapeutic trials of bile acid derivatives in CLD. In the near future, further evidence in this area might help clinicians better detect and manage liver diseases.

Indexed as

AD, Acute decompensationALP, Alkaline phosphataseAMACR, α-methylacyl-CoA racemase (AMACR)ASBT, Apical sodium dependent bile salt transporterBA, Bile acidbile acidsBSEP, Bile salt export pumpBSH, Bile salt hydrolaseCA, Cholic acidCDCA, Chenodeoxycholic acidcirrhosisCLDCLD, Chronic Liver DiseaseCTP, Child-Turcotte-PughCYP7A1, Cholesterol 7 α hydroxylaseDCA, Deoxycholic acidDR5, Death receptor 5ELF, Enhanced Liver FibrosisFGF-19, Fibroblast growth factor-19FGFR4, FGF receptor 4FXR, Farnesoid X receptorGCA, Glycocholic acidGDCA, Glycodeoxycholic acidGLP-1, Glucagon-like peptide1HBV, Hepatitis B virusHCV, Hepatitis C virusHVPG, Hepatic Venous Pressure GradientLCA, Lithocholic acidLPS, LipopolysaccharideMELD, Model for End-Stage Liver Disease (MELD)microbiomeMRI-PDFF, Magnetic resonance imaging derived proton density fat fractionNAFLDNAFLD, Non-alcoholic fatty liver diseaseNASH, Nonalcoholic steatohepatitisNAS, NAFLD activity scoreNTCP, Sodium taurocholate cotransporting polypeptideOCA, Obeticholic acidOST, Organic solute transporterPBC, Primary biliary cirrhosisPFIC, Progressive familial intrahepatic cholestasisPSC, Primary sclerosing cholangitisPXR, Pregnane X receptorSHP, Small heterodimer partnerTBA, Total bile acidsTGR5, Takeda G-protein coupled receptor 5TRAIL, TNF-related apoptosis-inducing ligandUDCA, Ursodeoxycholic acidUPLC-MS, Ultra-performance liquid chromatography with tandem mass spectrometryVDR, Vitamin D receptor

Identifiers

PMID35068796
PMCPMC8766695
OpenAlexW3194826249

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.