Evidence map›Paper›PMID 30988739›Full record

ArticleExperimental and therapeutic medicine2019

Glucagon-like peptide-1 modulates RAW264.7 macrophage polarization by interfering with the JNK/STAT3 signaling pathway.

Shan Wan, Hui Sun

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

46 citing papers in PubMed, 50 citations in OpenAlex.

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  10. The potential role of GLP-1 receptor agonists in the management of psoriatic disease: a scoping review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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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

2 authors at 2 institutions in 1 country.

Shan WanDepartment of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Hui SunDepartment of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China.
Huazhong University of Science and Technology · CNUnion Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin resistance and metabolic disorders are closely associated with low-grade chronic inflammation. Aberrant macrophage activation to M1 or M2 is characterized by a deleterious state of chronic inflammation and loss of positive trophic signals. Glucagon-like peptide-1 (GLP-1) is used to treat diabetes due to its beneficial role against insulin resistance. The present study examined the effect of GLP-1 on macrophage activation, which contributed to M2 polarization and secretion of anti-inflammatory factors. In addition, the present study demonstrated that GLP-1 was able to reduce M1 polarization and inflammatory response by using the murine monocyte/macrophage cell line RAW264.7 and detecting M1/M2-specific genes. RAW264.7 cells were incubated with GLP-1 in the presence or absence of lipopolysaccharide or interleukin-4, the c-Jun N-terminal kinase (JNK) and signal transduction and transcriptional activation factor 3 (STAT3) activity was assessed by quantification of phosphorylation expression and macrophage polarization was determined by detecting M1/M2-specific genes expression. The results demonstrated that GLP-1/GLP-1 receptor attenuated the phosphorylation of JNK and its signal transduction through the cyclic adenosine monophosphate/protein kinase A signaling pathway, while the phosphorylation of STAT3 increased through following treatment with GLP-1. The present study observed that GLP-1 exerts its beneficial effects on macrophage polarization by modulating the JNK/STAT3 signaling pathway. The present results also suggested that the effects of GLP-1 on endocrine and metabolic diseases are possibly mediated by modulation of signaling pathways, and provide a basis for pharmacologic targeting of macrophage activation and an insight into the molecular mechanisms involved in the progression of metabolic diseases.

Indexed as

c-Jun N-terminal kinaseglucagon-like peptide-1inflammatory signalingM1/M2 macrophagemetabolismsignal transduction and transcriptional activation factor 3

Identifiers

PMID30988739
PMCPMC6447820
OpenAlexW2919579975

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

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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.