Evidence map›Paper›PMID 32496563›Full record

ReviewEndocrinology2020

LXRα Phosphorylation in Cardiometabolic Disease: Insight From Mouse Models.

Maud Voisin, Matthew C Gage, Natalia Becares, Elina Shrestha, Edward A Fisher, Ines Pineda-Torra, Michael J Garabedian

Open access · bronzeAbstract readReview
In one paragraph

Review in Endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

6 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Liver X receptors and liver physiology.Biochimica et biophysica acta. Molecular basis of disease · 2021
    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

7 authors at 3 institutions in 2 countries.

Maud VoisinDepartment of Microbiology, New York University School of Medicine, New York, New York, US.
Matthew C GageDepartment of Comparative Biomedical Sciences, Royal Veterinary College, London, UK.
Natalia BecaresCentre of Clinical Pharmacology, Division of Medicine, University College of London, London, UK.
Elina ShresthaDepartment of Microbiology, New York University School of Medicine, New York, New York, US.
Edward A FisherDepartment of Microbiology, New York University School of Medicine, New York, New York, US.
Ines Pineda-TorraCentre of Cardiometabolic and Vascular Science, Division of Medicine, University College of London, London, UK.
Michael J GarabedianDepartment of Microbiology, New York University School of Medicine, New York, New York, US.
University School · USUniversity College London · GBRoyal Veterinary College · GB

Funding

Resolving Macrophage Inflammation in Atherosclerotic Plaques and Other Sites in Insulin ResistanceP01HL131481 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANN MARIE SCHMIDT · 2017 to 2026
$27.3M
Molecular Regulation of Atherosclerosis Regression - RenewalR01HL084312 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A · 2006 to 2024
$11.4M
Regulation of LXR alpha by glucose & cholesterol in diabetes & atherosclerosisR01HL117226 · NHLBI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI FISHER, EDWARD A, GARABEDIAN, MICHAEL J. · 2014 to 2017
$2.1M
British Heart Foundation PG/13/10/30000British Heart Foundation PG/16/87/32492Medical Research Council G0801278NHLBI NIH HHS P01 HL131481NHLBI NIH HHS R01 HL084312NHLBI NIH HHS R01 HL117226
6 · The paper itself

Abstract

Posttranslational modifications, such as phosphorylation, are a powerful means by which the activity and function of nuclear receptors such as LXRα can be altered. However, despite the established importance of nuclear receptors in maintaining metabolic homeostasis, our understanding of how phosphorylation affects metabolic diseases is limited. The physiological consequences of LXRα phosphorylation have, until recently, been studied only in vitro or nonspecifically in animal models by pharmacologically or genetically altering the enzymes enhancing or inhibiting these modifications. Here we review recent reports on the physiological consequences of modifying LXRα phosphorylation at serine 196 (S196) in cardiometabolic disease, including nonalcoholic fatty liver disease, atherosclerosis, and obesity. A unifying theme from these studies is that LXRα S196 phosphorylation rewires the LXR-modulated transcriptome, which in turn alters physiological response to environmental signals, and that this is largely distinct from the LXR-ligand-dependent action.

Indexed as

Disease Models, AnimalAnimalsAtherosclerosisLiver X ReceptorsMetabolic SyndromeMiceMolecular Targeted TherapyNon-alcoholic Fatty Liver DiseaseObesityPhosphorylationProtein Serine-Threonine KinasesLiver X ReceptorsProtein Serine-Threonine Kinasesatherosclerosisliver X receptorsNAFLDnuclear receptorsobesityphosphorylationtranscription

Identifiers

PMID32496563
PMCPMC7324054
OpenAlexW3032585506

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.