Evidence map›Paper›PMID 40023513›Full record

ReviewMolecular pharmacology2025

Insights of direct and indirect regulation of PXR through phosphorylation in fatty liver disease.

Veronia Basaly, Anisha Bhattacharya, Grace L Guo

Abstract readReview
In one paragraph

Review in Molecular pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Review
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.

Veronia BasalyDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Environmental and Occupational Health Sciences Institute, Rutgers, The State University of New Jersey, New Brunswick, New Jersey.
Anisha BhattacharyaDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Environmental and Occupational Health Sciences Institute, Rutgers, The State University of New Jersey, New Brunswick, New Jersey.
Grace L GuoDepartment of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Environmental and Occupational Health Sciences Institute, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; Rutgers Center for Lipid Research, Rutgers, The State University of New Jersey, New Brunswick, New Jersey; VA New Jersey Health Care System, Veterans Administration Medical Center, East Orange, New Jersey. Electronic address: glg48@eohsi.rutgers.edu.

Funding

Gut-liver crosstalk by FGF15/19 in regulating xenobiotic nuclear receptor activationR01GM135258 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI GUO, GRACE L · 2020 to 2023
$1.4M
Tissue specific mechanism of FXR in suppressing bile-acid synthesisR01DK081343 · NIDDK · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GUO, GRACE L · 2008 to 2011
$1.3M
BLRD VA I01 BX002741NIDDK NIH HHS R01 DK081343NIGMS NIH HHS R01 GM135258NIH HHS DK122725NIH HHS ES007148NIH HHS ES029258NIH HHS GM093854NIH HHS GM135258
6 · The paper itself

Abstract

The pregnane X receptor (PXR), a ligand-activated nuclear receptor, regulates the transcription of several genes that encode many enzymes and transporters related to drug metabolism. PXR also performs an important role as a physiological sensor in the modulation of endobiotic metabolism for hormones, bile acids, cholesterol, fatty acids, and glucose. Dysregulation of these PXR-mediated pathways is implicated in the progression of metabolic dysfunction-associated steatohepatitis (MASH), contributing to the complex interplay of factors involved in chronic liver disease development and exacerbation affecting millions worldwide. This review highlights the current knowledge of PXR expression and its role in endobiotic metabolism related to MASH development, which is associated with diverse causes and dire outcomes. This review focuses on elucidating the molecular pathways associated with PXR activation directly or indirectly and PXR interaction with other regulatory factors. Although there is still much to comprehend about the intricate details of these pathways, the conclusion is drawn that PXR exerts a crucial role in the pathological and physiological pathways of hepatic cellular processes, which holds promise as a potential pharmacological target for exploring novel therapeutic approaches for MASH treatment and/or prevention. SIGNIFICANCE STATEMENT: The pregnane X receptor (PXR) plays a fundamental role in regulating gene expression involved in xenobiotic and endobiotic metabolism. Dysregulation of PXR-mediated pathways is related to the development of metabolic dysfunction-associated steatohepatitis. The ligand-independent pathways regulating PXR hepatic functions through phosphorylation shed light on possible indirect molecular mechanisms and pathways that regulate PXR activity and function. Understanding these pathways may provide insight into new pharmaceutical interventions for metabolic dysfunction-associated steatohepatitis development.

Indexed as

Fatty LiverPregnane X ReceptorAnimalsHumansLiverNon-alcoholic Fatty Liver DiseasePhosphorylationPregnane X ReceptorFibrosisLigand dependencyLipogenesisMetabolic dysfunction–associated steatohepatitisPhosphorylationPregnane X receptor

Identifiers

PMID40023513
PMCPMC13095439

What OpenQuestion holds

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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.