Evidence map›Paper›PMID 29626115›Full record

ArticleThe Journal of experimental medicine2018

Macrophage/microglial Ezh2 facilitates autoimmune inflammation through inhibition of Socs3.

Xingli Zhang, Yan Wang, Jia Yuan, Ni Li, Siyu Pei, Jing Xu, Xuan Luo, Chaoming Mao, Junli Liu, Tao Yu and 9 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 114 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
114citing papers in PubMed, 1 pooled it
7.3field-weighted citation impact, top 2% 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

114 citing papers in PubMed, 1 synthesis or guideline pooled it, 182 citations in OpenAlex.

  1. Pooled it
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  9. mScience advances · 2026
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  11. Knockdown of SOX4 attenuates sepsis myocardial injury by inhibiting the EZH2/H3K27me3/SOCS3 axis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
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54 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

19 authors at 6 institutions in 2 countries.

Xingli ZhangThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Yan WangThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Jia YuanThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Ni LiThe Key Laboratory of Stem Cell Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Siyu PeiThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Jing XuThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Xuan LuoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Chaoming MaoDepartment of Nuclear Medicine, The Affiliated Hospital of Jiangsu University, Zhenjiang, China.
Junli LiuThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Tao YuThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Shucheng GanThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.
Qianqian ZhengSchool of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Yinming LiangSchool of Laboratory Medicine, Xinxiang Medical University, Xinxiang, China.
Weixiang GuoState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Ju QiuThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-1543-5678
Gabriela ConstantinDepartment of Medicine, Section of General Pathology, University of Verona, Verona, Italy.
Jin JinLife Sciences Institute, Zhejiang University, Hangzhou, China.ORCID 0000-0001-7887-5972
Jun QinThe Key Laboratory of Stem Cell Biology, Chinese Academy of Sciences Center for Excellence in Molecular Cell Science, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China qinjun@sibs.ac.cn.ORCID 0000-0002-2263-128X
Yichuan XiaoThe Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Shanghai, China ycxiao@sibs.ac.cn.ORCID 0000-0001-7804-6971
Shanghai Institutes for Biological Sciences · CNJiangsu University · CNXinxiang Medical University · CNChinese Academy of Sciences · CNUniversity of Verona · ITZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone 3 Lys27 (H3K27) trimethyltransferase Ezh2 is implicated in the pathogenesis of autoimmune inflammation. Nevertheless, the role of Ezh2 in macrophage/microglial activation remains to be defined. In this study, we identified that macrophage/microglial H3K27me3 or Ezh2, rather than functioning as a repressor, mediates toll-like receptor (TLR)-induced proinflammatory gene expression, and therefore Ezh2 depletion diminishes macrophage/microglial activation and attenuates the autoimmune inflammation in dextran sulfate sodium-induced colitis and experimental autoimmune encephalomyelitis. Mechanistic characterizations indicated that

Indexed as

AnimalsColitisDextran SulfateEncephalomyelitis, Autoimmune, ExperimentalEnhancer of Zeste Homolog 2 ProteinEpigenesis, GeneticHistonesIndolesInflammationLysineMacrophagesMethylationMiceMicrogliaModels, BiologicalMyeloid Differentiation Factor 88Dextran SulfateEnhancer of Zeste Homolog 2 ProteinGSK-2816126HistonesIndolesLysineMyeloid Differentiation Factor 88PyridonesSuppressor of Cytokine Signaling 3 ProteinTNF Receptor-Associated Factor 6TRAF6 protein, mouse

Identifiers

PMID29626115
PMCPMC5940261
OpenAlexW2795964681

What OpenQuestion holds

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LicenceCC BY-NC-SA
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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.