Evidence map›Paper›PMID 33986196›Full record

ArticleJCI insight2021

miR-9-5p regulates immunometabolic and epigenetic pathways in β-glucan-trained immunity via IDH3α.

Haibo Su, Zhongping Liang, ShuFeng Weng, Chaonan Sun, Jiaxin Huang, TianRan Zhang, Xialian Wang, Shanshan Wu, Zhi Zhang, Yiqi Zhang and 2 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in JCI insight, 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 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. KDM4 Regulates the Glycolysis of Hemocytes in the Immune Priming ofInternational journal of molecular sciences · 2024
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  14. Viruses · 2022
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 2 institutions in 1 country.

Haibo SuThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Zhongping LiangDepartment of General Surgery, The Sixth Affiliated Hospital, Guangzhou Medical University, Qingyuan, China.
ShuFeng WengState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, China.
Chaonan SunThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Jiaxin HuangThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
TianRan ZhangState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, China.
Xialian WangThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Shanshan WuThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Zhi ZhangThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Yiqi ZhangThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Qing GongThe Sixth Affiliated Hospital, GMU-GIBH Joint School of Life Science, Guangzhou Medical University, Guangzhou, China.
Ying XuState Key Laboratory of Genetic Engineering, Institute of Genetics, School of Life Science, Fudan University, Shanghai, China.
Fudan University · CNState Key Laboratory of Genetic Engineering

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Trained immunity, induced by β-glucan in monocytes, is mediated by activating metabolic pathways that result in epigenetic rewiring of cellular functional programs; however, molecular mechanisms underlying these changes remain unclear. Here, we report a key immunometabolic and epigenetic pathway mediated by the miR-9-5p-isocitrate dehydrogenase 3α (IDH3α) axis in trained immunity. We found that β-glucan-trained miR-9-5p-/- monocytes showed decreased IL-1β, IL-6, and TNF-α production after LPS stimulation. Trained miR-9-5p-/- mice produced decreased levels of proinflammatory cytokines upon rechallenge in vivo and had worse protection against Candida albicans infection. miR-9-5p targeted IDH3α and reduced α-ketoglutarate (α-KG) levels to stabilize HIF-1α, which promoted glycolysis. Accumulating succinate and fumarate via miR-9-5p action integrated immunometabolic circuits to induce histone modifications by inhibiting KDM5 demethylases. β-Glucan-trained monocytes exhibited low IDH3α levels, and IDH3α overexpression blocked the induction of trained immunity by monocytes. Monocytes with IDH3α variants from autosomal recessive retinitis pigmentosa patients showed a trained immunity phenotype at immunometabolic and epigenetic levels. These findings suggest that miR-9-5p and IDH3α act as critical metabolic and epigenetic switches in trained immunity.

Indexed as

Animalsbeta-GlucansCandida albicansCandidiasisEpigenesis, GeneticFumaratesGlycolysisHypoxia-Inducible Factor 1, alpha SubunitImmunity, InnateImmunologic MemoryInterleukin-1betaInterleukin-6Isocitrate DehydrogenaseKetoglutaric AcidsLipopolysaccharidesMetabolic Networks and Pathwaysbeta-GlucansFumaratesHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitIL1B protein, mouseInterleukin-1betaInterleukin-6interleukin-6, mouseIsocitrate Dehydrogenaseisocitrate dehydrogenase 3, mouseKetoglutaric AcidsLipopolysaccharidesMicroRNAsMIRN9 microRNA, mouseSuccinic AcidTnf protein, mouseTumor Necrosis Factor-alphaImmunologyInflammationInnate immunityMonocytes

Identifiers

PMID33986196
PMCPMC8262351
OpenAlexW3160044532

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.