Evidence map›Paper›PMID 19617629›Full record

ArticleThe Journal of biological chemistry2009

Adiponectin inhibits pro-inflammatory signaling in human macrophages independent of interleukin-10.

Eduardo J Folco, Viviane Z Rocha, Marco López-Ilasaca, Peter Libby

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed
6.7field-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

77 citing papers in PubMed, 131 citations in OpenAlex.

  1. Trial
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  6. Tumor-Associated Macrophage in Breast Tumor Microenvironment.International journal of molecular sciences · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. The Role of Adipokines in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

17 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

4 authors at 2 institutions in 1 country.

Eduardo J FolcoDivision of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Viviane Z Rocha
Marco López-Ilasaca
Peter Libby
Brigham and Women's Hospital · USHarvard University · US

Funding

Inflammatory Mechanisms of AtherosclerosisR01HL034636 · NHLBI · TUFTS UNIVERSITY BOSTON · PI LIBBY, PETER · 1985 to 2006
$1.9M
NHLBI NIH HHS R01 HL034636NHLBI NIH HHS R01-HL034636NHLBI NIH HHS R01-HL0831554
6 · The paper itself

Abstract

Macrophages participate pivotally in the pathogenesis of many chronic inflammatory diseases including atherosclerosis. Adiponectin, a vasculoprotective molecule with insulin-sensitizing and anti-atherogenic properties, suppresses pro-inflammatory gene expression in macrophages by mechanisms that remain incompletely understood. This study investigated the effects of adiponectin on major pro-inflammatory signaling pathways in human macrophages. We demonstrate that pretreatment of these cells with adiponectin inhibits phosphorylation of nuclear factor kappaB inhibitor (IkappaB), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK), induced by either lipopolysaccharide (LPS) or tumor necrosis factor (TNF) alpha, as well as STAT3 phosphorylation induced by interleukin-6 (IL6). Antagonism of IL10 by either neutralizing antibodies or siRNA-mediated silencing did not abrogate the anti-inflammatory actions of adiponectin, indicating that the ability of adiponectin to render human macrophages tolerant to various pro-inflammatory stimuli does not require this cytokine. A systematic search for adiponectin-inducible genes with established anti-inflammatory properties revealed that adiponectin augmented the expression of A20, suppressor of cytokine signaling (SOCS) 3, B-cell CLL/lymphoma (BCL) 3, TNF receptor-associated factor (TRAF) 1, and TNFAIP3-interacting protein (TNIP) 3. These results suggest that adiponectin triggers a multifaceted response in human macrophages by inducing the expression of various anti-inflammatory proteins that act at different levels in concert to suppress macrophage activation.

Indexed as

AdiponectinB-Cell Lymphoma 3 ProteinCell LineDNA-Binding ProteinsGene Expression RegulationHumansI-kappa B ProteinsInflammationInterleukin-10Interleukin-6Intracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLipopolysaccharidesMacrophagesMAP Kinase Signaling SystemNuclear ProteinsAdiponectinADIPOQ protein, humanB-Cell Lymphoma 3 ProteinBCL3 protein, humanDNA-Binding ProteinsI-kappa B ProteinsIL10 protein, humanIL6 protein, humanInterleukin-10Interleukin-6Intracellular Signaling Peptides and ProteinsJNK Mitogen-Activated Protein KinasesLipopolysaccharidesNuclear Proteinsp38 Mitogen-Activated Protein KinasesProteinsProto-Oncogene ProteinsSTAT3 protein, humanSTAT3 Transcription FactorTNFAIP3 protein, humanTNF Receptor-Associated Factor 1TNIP3 protein, humanTranscription FactorsTumor Necrosis Factor-alphaTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID19617629
PMCPMC2757958
OpenAlexW2000265203

What OpenQuestion holds

Textmetadata
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.