Evidence map›Paper›PMID 18366990›Full record

ReviewCurrent atherosclerosis reports2008

Liver X receptors as therapeutic targets in metabolism and atherosclerosis.

Takashi Nomiyama, Dennis Bruemmer

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
6.1field-weighted citation impact, top 4% 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

7 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Review
  5. Article
  6. Cytosolic sulfotransferase 2B1b promotes hepatocyte proliferation gene expression in vivo and in vitro.American journal of physiology. Gastrointestinal and liver physiology · 2012
    Article
  7. Mammalian Sirt1: insights on its biological functions.Cell communication and signaling : CCS · 2011
    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.

Takashi NomiyamaDivision of Endocrinology and Molecular Medicine, Department of Internal Medicine, University of Kentucky College of Medicine, Wethington Health Sciences Building, Room 575, 900 South Limestone Street, Lexington, KY 40536, USA.
Dennis Bruemmer
University of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The liver X receptors (LXRs) are ligand-activated transcription factors belonging to the nuclear hormone receptor superfamily. Since their initial identification more than a decade ago, LXRs have been characterized as key transcriptional regulators of lipid and carbohydrate homeostasis. LXRs are activated by the intracellular accumulation of cholesterol derivatives to stimulate cholesterol efflux and reverse cholesterol transport and excretion into the bile. Glucose functions as an LXR ligand in carbohydrate metabolism, and receptor agonism suppresses hepatic gluconeogenesis and improves insulin sensitivity. In addition to these beneficial metabolic effects, LXR ligands suppress inflammatory and proliferative responses of vascular cells and prevent the development of atherosclerosis and its complications. In this review, we summarize the important roles of LXRs in metabolism and vascular biology and discuss their implications as potential molecular drug targets for the treatment of cardiovascular diseases.

Indexed as

AnimalsApoptosisAtherosclerosisCell ProliferationCholesterolDNA-Binding ProteinsHumansIntestinal AbsorptionLipoproteins, HDLLiver X ReceptorsMacrophagesMyocytes, Smooth MuscleOrphan Nuclear ReceptorsReceptors, Cytoplasmic and NuclearTriglyceridesCholesterolDNA-Binding ProteinsLipoproteins, HDLLiver X ReceptorsOrphan Nuclear ReceptorsReceptors, Cytoplasmic and NuclearTriglycerides

Identifiers

PMID18366990
OpenAlexW2067212422

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.