Evidence map›Paper›PMID 23835343›Full record

ArticleDiabetes2013

Interferon regulatory factor 4 regulates obesity-induced inflammation through regulation of adipose tissue macrophage polarization.

Jun Eguchi, Xingxing Kong, Masafumi Tenta, Xun Wang, Sona Kang, Evan D Rosen

Open access · hybridAbstract read
In one paragraph

Article in Diabetes, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed, 1 pooled it
5.9field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 1 synthesis or guideline pooled it, 128 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. CAMKIIδ Reinforces Lipid Metabolism and Promotes the Development of B Cell Lymphoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  8. Review
  9. Review
  10. The role of interferon regulatory factors in atherosclerosis.Frontiers in cardiovascular medicine · 2025
    Review
  11. Review
  12. Review
  13. Review
  14. The Role of Interferon Regulatory Factors in Liver Diseases.International journal of molecular sciences · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

18 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 2 countries.

Jun EguchiDivision of Endocrinology, Beth Israel Deaconess Medical Center, Boston, Massachusetts.
Xingxing Kong
Masafumi Tenta
Xun Wang
Sona Kang
Evan D Rosen
Beth Israel Deaconess Medical Center · USOkayama University · JPHarvard University · US

Funding

REGULATION OF NUTRIENT HOMEOSTASIS BY IRF4R01DK085171 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2010 to 2018
$3.7M
Novel Transcriptional Pathways in AdipogenesisR01DK063906 · NIDDK · BETH ISRAEL DEACONESS MEDICAL CENTER · PI ROSEN, EVAN D · 2003 to 2007
$1.8M
NIDDK NIH HHS R01 DK063906NIDDK NIH HHS R01 DK085171NIDDK NIH HHS R01-DK-085171NIDDK NIH HHS R01-DK-63906
6 · The paper itself

Abstract

Interferon regulatory factors (IRFs) play functionally diverse roles in the transcriptional regulation of the immune system. We have previously shown that several IRFs are regulators of adipogenesis and that IRF4 is a critical transcriptional regulator of adipocyte lipid handling. However, the functional role of IRF4 in adipose tissue macrophages (ATMs) remains unclear, despite high expression there. Here we show that IRF4 expression is regulated in primary macrophages and in ATMs of high-fat diet-induced obese mice. Irf4(-/-) macrophages produce higher levels of proinflammatory cytokines, including interleukin-1β and tumor necrosis factor-α, in response to fatty acids. In coculture experiments, IRF4 deletion in macrophages leads to reduced insulin signaling and glucose uptake in 3T3-L1 adipocytes. To determine the macrophage-specific function of IRF4 in the context of obesity, we generated myeloid cell-specific IRF4 knockout mice, which develop significant insulin resistance on a high-fat diet, despite no difference in adiposity. This phenotype is associated with increased expression of inflammatory genes and decreased insulin signaling in adipose tissue, skeletal muscle, and liver. Furthermore, Irf4(-/-) ATMs express markers suggestive of enhanced M1 polarization. These findings indicate that IRF4 is a negative regulator of inflammation in diet-induced obesity, in part through regulation of macrophage polarization.

Indexed as

Cell Polarity3T3-L1 CellsAdipose TissueAnimalsBlotting, WesternCells, CulturedDiet, High-FatGlucoseGlucose Tolerance TestInflammationInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-1betaMacrophagesMiceMice, Inbred C57BLGlucoseInterferon Regulatory Factor-4Interferon Regulatory FactorsInterleukin-1betaTumor Necrosis Factor-alpha

Identifiers

PMID23835343
PMCPMC3781469
OpenAlexW2132067866

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.