Evidence map›Paper›PMID 34608215›Full record

ArticleScientific reports2021

Anti-inflammatory role of Gpnmb in adipose tissue of mice.

Bernadette Nickl, Fatimunnisa Qadri, Michael Bader

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  4. Lack of GPNMB Is Associated With Altered Lipid and Glucose Metabolism and Disrupted Diurnal Hepatic Glycogen Regulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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  20. Adipose Tissue Macrophages.Results and problems in cell differentiation · 2024
    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 at 2 institutions in 1 country.

Bernadette NicklMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association, Robert-Rössle-Str. 10, 13125, Berlin, Germany.
Fatimunnisa QadriMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association, Robert-Rössle-Str. 10, 13125, Berlin, Germany.
Michael BaderMax-Delbrück-Center for Molecular Medicine in the Helmholtz Association, Robert-Rössle-Str. 10, 13125, Berlin, Germany. mbader@mdc-berlin.de.
Berlin Institute of Health at Charité - Universitätsmedizin Berlin · DEMax Delbrück Center · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity can cause a chronic, low-grade inflammation, which is a critical step in the development of type II diabetes and cardiovascular diseases. Inflammation is associated with the expression of glycoprotein nonmetastatic melanoma protein b (Gpnmb), which is mainly expressed by macrophages and dendritic cells. We generated a Gpnmb-knockout mouse line using Crispr-Cas9 to assess the role of Gpnmb in a diet-induced obesity. The absence of Gpnmb did not affect body weight gain and blood lipid parameters. While wildtype animals became obese but remained otherwise metabolically healthy, Gpnmb-knockout animals developed, in addition to obesity, symptoms of metabolic syndrome such as adipose tissue inflammation, insulin resistance and liver fibrosis. We observed a strong Gpnmb expression in adipose tissue macrophages in wildtype animals and a decreased expression of most macrophage-related genes independent of their inflammatory function. This was corroborated by in vitro data showing that Gpnmb was mostly expressed by reparative macrophages while only pro-inflammatory stimuli induced shedding of Gpnmb. The data suggest that Gpnmb is ameliorating adipose tissue inflammation independent of the polarization of macrophages. Taken together, the data suggest an immune-balancing function of Gpnmb that could delay the metabolic damage caused by the induction of obesity.

Indexed as

Adipose TissueAnimalsBiomarkersDisease Models, AnimalDisease SusceptibilityEye ProteinsGene Expression RegulationInflammationInsulin ResistanceLiver CirrhosisMacrophagesMembrane GlycoproteinsMiceMice, KnockoutBiomarkersEye ProteinsGpnmb protein, mouseMembrane Glycoproteins

Identifiers

PMID34608215
PMCPMC8490452
OpenAlexW3202776049

What OpenQuestion holds

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LicenceCC BY
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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.