Evidence map›Paper›PMID 27066907›Full record

ArticleNature communications2016

FNDC4 acts as an anti-inflammatory factor on macrophages and improves colitis in mice.

Madeleen Bosma, Marco Gerling, Jenny Pasto, Anastasia Georgiadi, Evan Graham, Olga Shilkova, Yasunori Iwata, Sven Almer, Jan Söderman, Rune Toftgård and 3 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.

  1. Pooled it
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  17. Drug Repurposing using consilience of Knowledge Graph Completion methods.bioRxiv : the preprint server for biology · 2024
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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

13 authors at 4 institutions in 2 countries.

Madeleen BosmaDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Marco GerlingDepartment of Biosciences and Nutrition, Center of Innovative Medicine, Karolinska Institutet, Huddinge SE-141 83, Sweden.
Jenny PastoDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Anastasia GeorgiadiDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Evan GrahamDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Olga ShilkovaDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Yasunori IwataDivision of Nephrology, Kanazawa University Hospital, Kanazawa 920-8641, Japan.
Sven AlmerDepartment of Medicine, Solna, Karolinska Institutet, and Karolinska University Hospital, Stockholm SE-171 76, Sweden.
Jan SödermanDivision of Medical Diagnostics, Ryhov County Hospital, Jönköping 55185, Sweden.
Rune ToftgårdDepartment of Biosciences and Nutrition, Center of Innovative Medicine, Karolinska Institutet, Huddinge SE-141 83, Sweden.
Fredrik WermelingDepartment of Medicine, Solna, Karolinska Institutet, and Karolinska University Hospital, Stockholm SE-171 76, Sweden.
Elisabeth Almer BoströmDepartment of Dental Medicine, Karolinska Institutet, Huddinge SE-141 83, Sweden.
Pontus Almer BoströmDepartment of Cell and Molecular Biology, Karolinska Institutet, Stockholm SE-171 77, Sweden.
Karolinska Institutet · SEKanazawa University Hospital · JPKarolinska University Hospital · SERyhov Hospital Jönköping · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

FNDC4 is a secreted factor sharing high homology with the exercise-associated myokine irisin (FNDC5). Here we report that Fndc4 is robustly upregulated in several mouse models of inflammation as well as in human inflammatory conditions. Specifically, FNDC4 levels are increased locally at inflamed sites of the intestine of inflammatory bowel disease patients. Interestingly, administration of recombinant FNDC4 in the mouse model of induced colitis markedly reduces disease severity compared with mice injected with a control protein. Conversely, mice lacking Fndc4 develop more severe colitis. Analysis of binding of FNDC4 to different immune cell types reveals strong and specific binding to macrophages and monocytes. FNDC4 treatment of bone marrow-derived macrophages in vitro results in reduced phagocytosis, increased cell survival and reduced proinflammatory chemokine expression. Hence, treatment with FNDC4 results in a state of dampened macrophage activity, while enhancing their survival. Thus, we have characterized FNDC4 as a factor with direct therapeutic potential in inflammatory bowel disease and possibly other inflammatory diseases.

Indexed as

Amino Acid SequenceAnimalsAnti-Inflammatory AgentsCells, CulturedColitisDextran SulfateDisease ProgressionFibronectinsGene Expression RegulationHumansIntestinal MucosaMacrophagesMaleMembrane ProteinsMice, Inbred C57BLMice, KnockoutAnti-Inflammatory AgentsDextran SulfateFibronectinsFNDC4 protein, humanFNDC4 protein, mouseMembrane ProteinsProteinsSTAT3 Transcription FactorTransforming Growth Factor beta

Identifiers

PMID27066907
PMCPMC4832079
OpenAlexW2339102023

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.