Evidence map›Paper›PMID 21193034›Full record

ReviewBiochimica et biophysica acta2011

Role of nuclear receptor corepressor RIP140 in metabolic syndrome.

Meritxell Rosell, Marius C Jones, Malcolm G Parker

Open access · greenAbstract readReview
In one paragraph

Review in Biochimica et biophysica acta, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  9. Deletion of Nrip1 Extends Female Mice Longevity, Increases Autophagy, and Delays Cell Senescence.The journals of gerontology. Series A, Biological sciences and medical sciences · 2018
    Article
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  13. Review
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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 2 institutions in 1 country.

Meritxell RosellInstitute of Reproductive and Developmental Biology, Imperial College London, Faculty of Medicine, Hammersmith Campus 158 Du Cane Road, W12 0NN, UK. m.parker@imperial.ac.uk
Marius C Jones
Malcolm G Parker
Imperial College London · GBHammersmith Hospital · GB

Funding

Biotechnology and Biological Sciences Research Council 504327Wellcome Trust 079200/Z/06/Z
6 · The paper itself

Abstract

Obesity and its associated complications, which can lead to the development of metabolic syndrome, are a worldwide major public health concern especially in developed countries where they have a very high prevalence. RIP140 is a nuclear coregulator with a pivotal role in controlling lipid and glucose metabolism. Genetically manipulated mice devoid of RIP140 are lean with increased oxygen consumption and are resistant to high-fat diet-induced obesity and hepatic steatosis with improved insulin sensitivity. Moreover, white adipocytes with targeted disruption of RIP140 express genes characteristic of brown fat including CIDEA and UCP1 while skeletal muscles show a shift in fibre type composition enriched in more oxidative fibres. Thus, RIP140 is a potential therapeutic target in metabolic disorders. In this article we will review the role of RIP140 in tissues relevant to the appearance and progression of the metabolic syndrome and discuss how the manipulation of RIP140 levels or activity might represent a therapeutic approach to combat obesity and associated metabolic disorders. This article is part of a Special Issue entitled: Translating nuclear receptors from health to disease.

Indexed as

Adaptor Proteins, Signal TransducingAdipose TissueAnimalsHumansInflammationMetabolic SyndromeMusclesNuclear ProteinsNuclear Receptor Interacting Protein 1Adaptor Proteins, Signal TransducingNRIP1 protein, humanNuclear ProteinsNuclear Receptor Interacting Protein 1

Identifiers

PMID21193034
PMCPMC3117993
OpenAlexW2143958727

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.