Evidence map›Paper›PMID 26285907›Full record

ArticleThe Journal of endocrinology2015

STAT4 contributes to adipose tissue inflammation and atherosclerosis.

A D Dobrian, M A Hatcher, J J Brotman, E V Galkina, P Taghavie-Moghadam, H Pei, B A Haynes, J L Nadler

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of endocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-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

17 citing papers in PubMed, 26 citations in OpenAlex.

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  7. Interaction between theAnnals of the rheumatic diseases · 2021
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  13. Epigenetics and Immunometabolism in Diabetes and Aging.Antioxidants & redox signaling · 2018
    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

8 authors at 3 institutions in 2 countries.

A D DobrianDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA dobriaad@evms.edu.
M A HatcherDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
J J BrotmanDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
E V GalkinaDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
P Taghavie-MoghadamDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
H PeiDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
B A HaynesDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
J L NadlerDepartments of Physiological SciencesMicrobiology and Molecular Cell BiologyInternal MedicineEastern Virginia Medical School, 700W Olney Road, Norfolk, Virginia 23505, USADivision of Inflammation BiologyLa Jolla Institute for Allergy and Immunology, San Diego, La Jolla, California, USA.
Eastern Virginia Medical School · USInstitute of Molecular and Cell Biology · RULa Jolla Institute for Immunology · US

Funding

ROLE OF LIPOXYGENASES IN ATHEROGENESIS IN DIABETES MELLITUSP01HL055798 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI TAYLOR, ANGELA M · 1995 to 2016
$28.4M
Role of the Interleukin12/STAT4 Pathway in Insulin Resistance and AtherosclerosisR01HL112605 · NHLBI · EASTERN VIRGINIA MEDICAL SCHOOL · PI NADLER, JERRY L. · 2012 to 2016
$2.0M
NHLBI NIH HHS P01 HL055798NHLBI NIH HHS P01 HL55798NHLBI NIH HHS R01 HL112605
6 · The paper itself

Abstract

Adipose tissue (AT) inflammation is an emerging factor contributing to cardiovascular disease. STAT4 is a transcription factor expressed in adipocytes and in immune cells and contributes to AT inflammation and insulin resistance in obesity. The objective of this study was to determine the effect of STAT4 deficiency on visceral and peri-aortic AT inflammation in a model of atherosclerosis without obesity. Stat4(-/-)Apoe(-/-) mice and Apoe(-/-) controls were kept either on chow or Western diet for 12 weeks. Visceral and peri-aortic AT were collected and analyzed for immune composition by flow cytometry and for cytokine/chemokine expression by real-time PCR. Stat4(-/-)Apoe(-/-) and Apoe(-/-) mice had similar body weight, plasma glucose, and lipids. Western diet significantly increased macrophage, CD4+, CD8+, and NK cells in peri-aortic and visceral fat in Apoe(-/-) mice. In contrast, in Stat4(-/-)Apoe(-/-) mice, a Western diet failed to increase the percentage of immune cells infiltrating the AT. Also, IL12p40, TNFa, CCL5, CXCL10, and CX3CL1 were significantly reduced in the peri-aortic fat in Stat4(-/-)Apoe(-/-) mice. Importantly, Stat4(-/-)Apoe(-/-) mice on a Western diet had significantly reduced plaque burden vs Apoe(-/-) controls. In conclusion, STAT4 deletion reduces inflammation in peri-vascular and visceral AT and this may contribute via direct or indirect effects to reduced atheroma formation.

Indexed as

AnimalsAortaApolipoproteins EAtherosclerosisCell PolarityCells, CulturedChemokinesCytokinesDiet, WesternFemaleIntra-Abdominal FatMacrophagesMacrophages, PeritonealMice, KnockoutOvaryPanniculitisApolipoproteins EChemokinesCytokinesStat4 protein, mouseSTAT4 Transcription Factorchemokinesmacrophagesperi-aortic fatT lymphocytes

Identifiers

PMID26285907
PMCPMC4811759
OpenAlexW2202049421

What OpenQuestion holds

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LicenceTDM
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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.