Evidence map›Paper›PMID 34183017›Full record

ArticleJournal of neuroinflammation2021

Smek1 deficiency exacerbates experimental autoimmune encephalomyelitis by activating proinflammatory microglia and suppressing the IDO1-AhR pathway.

Ruo-Nan Duan, Chun-Lin Yang, Tong Du, Ai Liu, An-Ran Wang, Wen-Jie Sun, Xi Li, Jiang-Xia Li, Chuan-Zhu Yan, Qi-Ji Liu

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

13 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
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  3. Aryl hydrocarbon receptor (AhR) alleviates the LPS-induced inflammatory responses in IPEC-J2 cells by activating PINK1/Parkin-mediated mitophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Ruo-Nan DuanKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Chun-Lin YangDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Tong DuDepartment of Neurology, Shandong Provincial Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Ai LiuKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
An-Ran WangKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Wen-Jie SunKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Xi LiKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Jiang-Xia LiKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China.
Chuan-Zhu YanDepartment of Neurology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, People's Republic of China.
Qi-Ji LiuKey Laboratory for Experimental Teratology of the Ministry of Education and Department of Medical Genetics, Cheeloo College of Medicine, School of Basic Medical Sciences, Shandong University, No.44 West Wenhua Road, Jinan, Shandong, 250012, People's Republic of China. liuqiji@sdu.edu.cn.ORCID https://orcid.org/0000-0001-6321-4581
Shandong University · CNQilu Hospital of Shandong University · CN

Funding

China Postdoctoral Science Foundation funded project 2015M570598Fundamental Research Funds of Shandong University 2017JC008Key Research and Development Program of Shandong Province 2016ZDJS07A08, 2018CXGC1211National Natural Science Foundation of China 32070586, 81741055, 81873878Shandong Natural Science Foundation ZR2020QH097, 2015GSF118050, ZR2015HZ002, ZR2016HZ01, ZR2012HQ015
6 · The paper itself

Abstract

backgroundExperimental autoimmune encephalomyelitis (EAE) is an animal disease model of multiple sclerosis (MS) that involves the immune system and central nervous system (CNS). However, it is unclear how genetic predispositions promote neuroinflammation in MS and EAE. Here, we investigated how partial loss-of-function of suppressor of MEK1 (SMEK1), a regulatory subunit of protein phosphatase 4, facilitates the onset of MS and EAE.

methodsC57BL/6 mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG

resultsHere, we showed that partial Smek1 deficiency caused more severe symptoms in the EAE model than in controls by activating myeloid cells and that Smek1 was required for maintaining immunosuppressive function by modulating the indoleamine 2,3-dioxygenase (IDO1)-aryl hydrocarbon receptor (AhR) pathway. Single-cell sequencing and an in vitro study showed that Smek1-deficient microglia and macrophages were preactivated at steady state. After MOG

conclusionsThe present study suggests a protective role of Smek1 in autoimmune demyelination pathogenesis via immune suppression and inflammation regulation in both the immune system and the central nervous system. Our findings provide an instructive basis for the roles of Smek1 in EAE and broaden the understanding of the genetic factors involved in the pathogenesis of autoimmune demyelination.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalAnimalsCentral Nervous SystemCytokinesDisease Models, AnimalGene Knockout TechniquesIndoleamine-Pyrrole 2,3,-DioxygenaseInflammationInterferon-gammaMiceMice, Inbred C57BLMicrogliaMultiple SclerosisMyelin-Oligodendrocyte GlycoproteinMyeloid CellsPeptide FragmentsCytokinesIndoleamine-Pyrrole 2,3,-DioxygenaseInterferon-gammaMyelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsPhosphoprotein PhosphatasesPpp4r3a protein, mouseReceptors, Aryl HydrocarbonExperimental autoimmune encephalomyelitisIndoleamine 2,3-dioxygenaseInterleukin 1βMicrogliaSuppressor of MEK1

Identifiers

PMID34183017
PMCPMC8237434
OpenAlexW3173681446

What OpenQuestion holds

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LicenceCC BY
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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.