Evidence map›Paper›PMID 41296787›Full record

ArticlePloS one2025

TNFAIP3 alleviates cerebral ischemia-reperfusion injury by inhibiting M1 microglia polarization via deubiquitination of RACK1.

Wenya Bai, Shixuan Liu, Guilin Zhou, Xuelian Li, Huan Jiang, Jianlin Shao, Junchao Zhu

Abstract read
In one paragraph

Article in PloS one, 2025. 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

7 authors.

Wenya BaiDepartment of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, P. R. China.ORCID https://orcid.org/0000-0001-5329-2527
Shixuan LiuDepartment of Anesthesiology, The Shengjing Hospital of China Medical University, Shenyang, Liaoning, P. R. China.
Guilin ZhouDepartment of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, P. R. China.
Xuelian LiDepartment of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, P. R. China.
Huan JiangDepartment of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, P. R. China.
Jianlin ShaoDepartment of Anesthesiology, The First Affiliated Hospital of Kunming Medical University, Kunming, Yunnan, P. R. China.ORCID https://orcid.org/0000-0001-9878-7064
Junchao ZhuDepartment of Anesthesiology, The Shengjing Hospital of China Medical University, Shenyang, Liaoning, P. R. China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroglia polarization plays a crucial role in the progression of cerebral ischemia-reperfusion injury (CIRI), but the mechanisms remain largely undefined. The preset study aimed to investigate the mechanism of microglia polarization following CIRI.

methodsCIRI was modeled in C57BL/6J mice through middle cerebral artery occlusion-reperfusion and in BV2 cells via oxygen and glucose deprivation/reoxygenation. Reverse transcription-quantitative PCR, western blotting, flow cytometry and fluorescence staining were used to detect the expression levels of key proteins associated with microglia polarization, as well as the expression of TNFAIP3 and RACK1. The interaction between TNFAIP3 and RACK1 was verified by co-immunoprecipitation. TNFAIP3 or RACK1 gene interference (overexpression and/or silencing) was employed to examine the role of the TNFAIP3/RACK1 axis in microglia polarization following CIRI.

resultsThe results revealed that Arg-1 expression decreased, inducible nitric oxide synthase expression increased and TNFAIP3 was upregulated 24 h after CIRI. Furthermore, TNFAIP3 interacted with RACK1 to deubiquitinate and increase the expression of RACK1. These results indicate that knocking down either TNFAIP3 or RACK1 promotes microglia M1 polarization, and overexpression of RACK1 can promote microglia M2 polarization. RACK1 exerts its neuroprotective effects through NF-κB, as demonstrated by the use of NF-κB inhibitors.

conclusionThe present findings indicate that TNFAIP3 inhibits M1 microglial polarization via deubiquitination of RACK1 after CIRI, RACK1 exerts its effects through NF-κB.

Indexed as

Brain IschemiaMicrogliaReceptors for Activated C KinaseReperfusion InjuryTumor Necrosis Factor alpha-Induced Protein 3AnimalsArginaseCell LineCell PolarityMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIUbiquitinationArg1 protein, mouseArginaseNitric Oxide Synthase Type IIRACK1 protein, mouseReceptors for Activated C KinaseTnfaip3 protein, mouseTumor Necrosis Factor alpha-Induced Protein 3

Identifiers

PMID41296787
PMCPMC12654896

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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.