Evidence map›Paper›PMID 31962332›Full record

ArticleObesity facts2020

The Role of MKP-5 in Adipocyte-Macrophage Interactions during Obesity.

Yuanhua Lu, Jie Ma, Jianan Zhao, Zhuoyao Song, Chao Zhou, Xiu Liu, Wenjing Teng, Wei Wang, Qi Zhang, Weiqun Yan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Obesity facts, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

  1. MAP kinase phosphatases in metabolic diseases.Trends in endocrinology and metabolism: TEM · 2026
    Review
  2. Kinin receptors in adipose tissue: drivers of inflammation and metabolic dysfunction in obesity.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  3. Article
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  8. Dichotomous Roles ofInternational journal of molecular sciences · 2022
    Article
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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

11 authors at 1 institution in 1 country.

Yuanhua LuSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Jie MaSchool of Pharmaceutical Sciences, Jilin University, Changchun, China, ma_jie@jlu.edu.cn.
Jianan ZhaoSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Zhuoyao SongSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Chao ZhouSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Xiu LiuSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Wenjing TengSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Wei WangSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Qi ZhangSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Weiqun YanSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Ping JiaoSchool of Pharmaceutical Sciences, Jilin University, Changchun, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveIn obese individuals, chronic low-grade inflammation resulting from adipocyte-macrophage interactions is a major cause of adipose tissue dysfunction and metabolic disease. This study investigated the role of MAP kinase phosphatase-5 (MKP-5) in obesity-induced inflammation during macrophage and adipocyte interactions.

methodsHigh-fat diet-induced obese mice were used to explore the role of MKP-5 in obesity-induced adipose tissue inflammation. Macrophage polarization was determined by inflammatory cytokine expression in MKP-5-overexpressed or -silenced Raw264.7 cells exposed to palmitate (PA) or M1/M2 macrophage inducers. To uncover the role of MKP-5 during macrophage-adipocyte interactions, a coculture system composed of differentiated 3T3-L1 and Raw264.7 cells was employed. MAPK inhibitors were used to investigate the involvement of MAPK signaling.

resultsIncreased MKP-5 expression was observed in adipose stromal vascular cells (SVCs) of obese mice. In Raw264.7 cells, MKP-5 promoted the switching of M1 macrophages to an M2 phenotype. Notably, MKP-5 reduced inflammation during the interaction of macrophages and adipocytes. MKP-5 overexpression in primary SVCs attenuated the expression of inflammatory mediators and increased the number of obesity-induced adipose tissue macrophages. MKP-5 suppressed PA-induced inflammation through the inactivation of P38, JNK, and ERK MAPKs.

conclusionsMKP-5 promotes macrophages to switch from the M1 to the M2 phenotype and is an inflammatory inhibitor involved in obesity-induced adipose tissue inflammation and PA-triggered macrophage inflammation via the P38, JNK, and ERK MAPK pathways. MKP-5 may be developed into a potential therapeutic target for obesity-related diseases, including type 2 diabetes mellitus and insulin resistance.

Indexed as

3T3-L1 CellsAdipocytesAdipose TissueAnimalsCell CommunicationCoculture TechniquesDiet, High-FatDual-Specificity PhosphatasesHEK293 CellsHumansInsulin ResistanceMacrophagesMaleMiceMice, Inbred C57BLMice, ObeseDual-Specificity PhosphatasesDusp10 protein, mouseAdipocytesInflammationMacrophageMKP-5Obesity

Identifiers

PMID31962332
PMCPMC7098294
OpenAlexW3001754956

What OpenQuestion holds

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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.