Evidence map›Paper›PMID 32335773›Full record

ArticleCellular and molecular neurobiology2021

Knockdown of TRIM22 Relieves Oxygen-Glucose Deprivation/Reoxygenation-Induced Apoptosis and Inflammation Through Inhibition of NF-κB/NLRP3 Axis.

Chongyang Kang, Zhaofeng Lu, Gangyi Zhu, Yuehua Chen, Yafang Wu

Open access · greenAbstract read
In one paragraph

Article in Cellular and molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

  1. Review
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  4. The Roles of E3 Ubiquitin Ligases in Cerebral Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025
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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

5 authors at 1 institution in 1 country.

Chongyang KangDepartment of Emergency, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Zhaofeng LuDepartment of Emergency, First Affiliated Hospital of Henan University of Science and Technology, Luoyang, 471003, China. luzhaofeng_doc@163.com.
Gangyi ZhuDepartment of Emergency, First Affiliated Hospital of Henan University of Science and Technology, Luoyang, 471003, China.
Yuehua ChenDepartment of Emergency, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
Yafang WuDepartment of Emergency, First Affiliated Hospital, and College of Clinical Medicine of Henan University of Science and Technology, Luoyang, 471003, China.
First Affiliated Hospital of Henan University of Science and Technology · CN

Funding

High level cultivation fund of Henan University of Science and Technology 2015GJB021Project fund of science and technology department of henan province 164102310412
6 · The paper itself

Abstract

Tripartite motif-containing 22 (TRIM22) has been documented to participate in numerous cellular activities during human diseases. However, whether TRIM22 is involved in the regulation of neuronal survival during the progression of cerebral ischemia/reperfusion (I/R) injury remains unknown. In the present study, treatment of HCN-2 cells with oxygen-glucose deprivation/reoxygenation (OGD/R) markedly upregulated TRIM22 expression. A significant increase in TRIM22 expression was observed in the ischemic cortex tissues from middle cerebral artery occlusion/reperfusion mice. OGD/R inhibited the viability and induced the apoptosis of HCN-2 cells, which was accompanied by an increase in caspase-3 activity and an increase in LDH release. Furthermore, OGD/R increased the levels of tumor necrosis factor-alpha, interleukin (IL)-1 beta, IL-6, and monocyte chemoattractant protein-1 and induced NLRP3 inflammasome activation, as evidenced by increases in NACHT, LRR and PYD domains-containing protein 3, apoptosis-associated speck-like protein containing a caspase recruitment domain and cleaved caspase-1 expression and caspase-1 activity. However, these changes induced by OGD/R were blocked by silencing of TRIM22. In addition, TRIM22 regulated NF-κB activity in HCN-2 cells undergoing OGD/R stimulation. Furthermore, inhibition of NF-κB by pyrrolidine dithiocarbamate inhibited OGD/R-induced NLRP3 inflammasome activation in HCN-2 cells. Taken together, silencing of TRIM22 protects neurons against OGD/R-induced apoptosis and inflammation. The anti-inflammatory effect of TRIM22 knockdown was the consequence of inhibition of NF-κB/NLRP3 axis. TRIM22 may be a potential target for treating cerebral I/R injury.

Indexed as

ApoptosisAnimalsCell LineGene Knockdown TechniquesGlucoseInflammasomesInflammationMaleMiceMinor Histocompatibility AntigensNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxygenRepressor ProteinsSignal TransductionTripartite Motif ProteinsGlucoseInflammasomesMinor Histocompatibility AntigensNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOxygenRepressor ProteinsTRIM22 protein, humanTripartite Motif ProteinsCerebral ischemia/reperfusion injuryNuclear factor-κbNucleotide-binding oligomerization domain-like receptor pyrin domain containing 3Tripartite motif-containing 22

Identifiers

PMID32335773
PMCPMC11448583
OpenAlexW3019026301

What OpenQuestion holds

Textmetadata
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.