Evidence map›Paper›PMID 33912173›Full record

ArticleFrontiers in immunology2021

Taurine Antagonizes Macrophages M1 Polarization by Mitophagy-Glycolysis Switch Blockage

Ling Meng, Cailing Lu, Bin Wu, Chunhua Lan, Laiming Mo, Chengying Chen, Xinhang Wang, Ning Zhang, Li Lan, Qihui Wang and 3 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

40 citing papers in PubMed, 68 citations in OpenAlex.

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  18. Taurine corrects lupus CD4Nutrition & metabolism · 2025
    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

13 authors at 1 institution in 1 country.

Ling MengSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Cailing LuSchool of Public Health, Guangxi Medical University, Nanning, China.
Bin WuSchool of Public Health, Guangxi Medical University, Nanning, China.
Chunhua LanSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Laiming MoSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Chengying ChenSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Xinhang WangSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Ning ZhangSchool of Public Health, Guangxi Medical University, Nanning, China.
Li LanSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Qihui WangSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Xia ZengSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Xiyi LiSchool of Public Health, Guangxi Medical University, Nanning, China.
Shen TangSchool of Basic Medical Sciences, Guangxi Medical University, Nanning, China.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The excessive M1 polarization of macrophages drives the occurrence and development of inflammatory diseases. The reprogramming of macrophages from M1 to M2 can be achieved by targeting metabolic events. Taurine promotes for the balance of energy metabolism and the repair of inflammatory injury, preventing chronic diseases and complications. However, little is known about the mechanisms underlying the action of taurine modulating the macrophage polarization phenotype. In this study, we constructed a low-dose LPS/IFN-γ-induced M1 polarization model to simulate a low-grade pro-inflammatory process. Our results indicate that the taurine transporter TauT/SlC6A6 is upregulated at the transcriptional level during M1 macrophage polarization. The nutrient uptake signal on the membrane supports the high abundance of taurine in macrophages after taurine supplementation, which weakens the status of methionine metabolism, resulting in insufficient S-adenosylmethionine (SAM). The low availability of SAM is directly sensed by LCMT-1 and PME-1, hindering PP2Ac methylation. PP2Ac methylation was found to be necessary for M1 polarization, including the positive regulation of VDAC1 and PINK1. Furthermore, its activation was found to promote the elimination of mitochondria by macrophages

Indexed as

Gene ExpressionGlycolysisHumansInterferon-gammaLipopolysaccharidesMacrophage ActivationMacrophagesMembrane GlycoproteinsMembrane Potential, MitochondrialMembrane Transport ProteinsMethylationMitophagyProtein KinasesProtein Phosphatase 2PTEN-Induced Putative KinaseS-AdenosylmethionineInterferon-gammaLipopolysaccharidesMembrane GlycoproteinsMembrane Transport ProteinsProtein KinasesProtein Phosphatase 2PTEN-Induced Putative KinaseS-AdenosylmethionineTaurineTaurine TransportersVoltage-Dependent Anion Channel 1low-grade inflammationM1 macrophagemitophagyPP2Ac methylationSAMtaurine

Identifiers

PMID33912173
PMCPMC8071881
OpenAlexW3152933542

What OpenQuestion holds

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LicenceCC BY
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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.