Evidence map›Paper›PMID 18159925›Full record

ReviewMolecular pharmaceutics

Cell signaling and nuclear receptors: new opportunities for molecular pharmaceuticals in liver disease.

Jeff L Staudinger, Kristin Lichti

Open access · greenAbstract readReview
In one paragraph

Review in Molecular pharmaceutics. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. A SUMO-acetyl switch in PXR biology.Biochimica et biophysica acta · 2016
    Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Zinc and alcoholic liver disease.Digestive diseases (Basel, Switzerland) · 2010
    Review
  13. PGC-1alpha negatively regulates hepatic FGF21 expression by modulating the heme/Rev-Erb(alpha) axis.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  14. Article
  15. Bile acids as regulatory molecules.Journal of lipid research · 2009
    Review
  16. Article
  17. Article
  18. Article
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

2 authors at 1 institution in 1 country.

Jeff L StaudingerUniversity of Kansas, Department of Pharmacology and Toxicology, 1251 Wescoe Hall Dr, 5038 Malott Hall, Lawrence, Kansas 66045, USA. stauding@ku.edu
Kristin Lichti
University of Kansas · US

Funding

Cell Signaling, PXR Phosphorylation &Drug DispositionR01DK068443 · NIDDK · UNIVERSITY OF KANSAS LAWRENCE · PI STAUDINGER, JEFFREY L · 2005 to 2009
$1.3M
NIDDK NIH HHS R01 DK068443
6 · The paper itself

Abstract

Liver-enriched nuclear receptors (NRs) collectively function as metabolic and toxicological "sensors" that mediate liver-specific gene-activation in mammals. NR-mediated gene-environment interaction regulates important steps in the hepatic uptake, metabolism, and excretion of glucose, fatty acids, lipoproteins, cholesterol, bile acids, and xenobiotics. Hence, liver-enriched NRs play pivotal roles in the overall control of energy homeostasis in mammals. While it is well-recognized that ligand-binding is the primary mechanism behind activation of NRs, recent research reveals that multiple signal transduction pathways modulate NR-function in liver. The interface between specific signal transduction pathways and NRs helps to determine their overall responsiveness to various environmental and physiological stimuli. In general, phosphorylation of hepatic NRs regulates multiple biological parameters including their transactivation capacity, DNA binding, subcellular location, capacity to interact with protein-cofactors, and protein stability. Certain pathological conditions including inflammation, morbid obesity, hyperlipidemia, atherosclerosis, insulin resistance, and type-2 diabetes are known to modulate selected signal transduction pathways in liver. This review will focus upon recent insights regarding the molecular mechanisms that comprise the interface between disease-mediated activation of hepatic signal transduction pathways and liver-enriched NRs. This review will also highlight the exciting opportunities presented by this new knowledge to develop novel molecular and pharmaceutical strategies for combating these increasingly prevalent human diseases.

Indexed as

Cell CommunicationSignal TransductionAnimalsDrugs, InvestigationalHumansLiver DiseasesReceptors, Cytoplasmic and NuclearDrugs, InvestigationalReceptors, Cytoplasmic and Nuclear

Identifiers

PMID18159925
PMCPMC2387130
OpenAlexW1993662329

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.