Evidence map›Paper›PMID 41719238›Full record

ArticlePloS one2026

A new mechanism regulating microglial NLRP3 inflammasome: FMR1 mediates NLRP3 mRNA stability.

Qian Deng, Qianqian Bai, Yang Yang, Wenchao Tang, Fangfei Liu, Shumin Zhang, Hao Wang, Zhehua Xing, Chi Zhang, Yanhui Yang and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
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

12 authors.

Qian DengDepartment of Pharmacy, Luoyang Central Hospital Affiliated to Zhengzhou University, Luoyang, China.
Qianqian BaiThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Yang YangThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Wenchao TangThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Fangfei LiuThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Shumin ZhangThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Hao WangThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Zhehua XingThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Chi ZhangThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Yanhui YangDepartment of Trauma center, The First Affiliated Hospital, College of Clinical Medicine, Henan University of Science and Technology, Luoyang, China.
Qizhi FuDepartment of Intensive Care Unit (Internal Medicine), The First Affiliated Hospital, And College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.
Hua FanThe First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, China.ORCID https://orcid.org/0000-0002-4333-2473

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe NLRP3 inflammasome drives chronic inflammation and contributes to the pathogenesis of multiple sclerosis (MS). This study aimed to elucidate a novel post-transcriptional regulatory mechanism controlling NLRP3 expression in microglia under lipopolysaccharide (LPS) stimulation.

methodsThe experimental autoimmune encephalomyelitis (EAE) mouse model of MS was established and divided into four groups: Sham, EAE, EAE + Lv-con (control lentivirus), and EAE + Lv-FMR1 (FMR1-overexpressing lentivirus). BV2 microglial cells were stimulated with LPS and adenosine triphosphate (ATP). mRNA and protein levels were assessed by qPCR, western blot, immunofluorescence, and immunohistochemistry. Caspase-1 activity and IL-1β/IL-18 levels were quantified using commercial assay kits. RNA-binding proteins (RBPs) interacting with NLRP3 mRNA were identified by RNA pull-down combined with mass spectrometry. NLRP3 mRNA stability was analyzed using Actinomycin D.

resultsNLRP3 inflammasome activation was confirmed in the spinal cords of EAE mice and in LPS/ATP-stimulated BV2 cells. Lentivirus-mediated overexpression of FMR1 in EAE mice attenuated microglial activation (reduced IBA-1) and decreased NLRP3 expression compared to the EAE + Lv-con control group. Immunohistochemistry confirmed reduced caspase-1 deposition in the EAE + Lv-FMR1 group. Mechanistically, FMR1 directly interacted with the 3' untranslated region (3'UTR) of NLRP3 mRNA in LPS/ATP-treated BV2 cells, leading to mRNA destabilization and consequent suppression of NLRP3 protein expression. Functionally, FMR1 inhibited NLRP3 inflammasome activation by downregulating NLRP3.

conclusionFMR1 suppresses NLRP3 inflammasome activation in both EAE mice and microglial cell models by destabilizing NLRP3 mRNA. This suggests that FMR1 possesses therapeutic potential for MS by dually regulating neuroinflammation and NLRP3-driven pathology.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalFragile X Messenger Ribonucleoprotein 1InflammasomesMicrogliaNLR Family, Pyrin Domain-Containing 3 ProteinRNA StabilityAnimalsCaspase 1Cell LineFemaleInterleukin-1betaLipopolysaccharidesMiceMice, Inbred C57BLMultiple SclerosisRNA, MessengerCaspase 1Fragile X Messenger Ribonucleoprotein 1InflammasomesInterleukin-1betaLipopolysaccharidesNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseRNA, Messenger

Identifiers

PMID41719238
PMCPMC12922985

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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.