Evidence map›Paper›PMID 34059091›Full record

ReviewJournal of neuroinflammation2021

Relevant mediators involved in and therapies targeting the inflammatory response induced by activation of the NLRP3 inflammasome in ischemic stroke.

Qingxue Xu, Bo Zhao, Yingze Ye, Yina Li, Yonggang Zhang, Xiaoxing Xiong, Lijuan Gu

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Journal of neuroinflammation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

62 citing papers in PubMed, 111 citations in OpenAlex.

  1. Review
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  11. Interactive effects of morphine and the HIV integrase inhibitor, cabotegravir, in male and female mice.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
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  12. Review
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  15. The Extract ofCurrent neuropharmacology · 2025
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  20. Article

2 more citing papers are in PubMed but not listed here.

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 at 2 institutions in 1 country.

Qingxue Xu *Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Bo Zhao *Department of Anesthesiology, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Yingze YeCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Yina LiCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Yonggang ZhangCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China.
Xiaoxing XiongCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China. xiaoxingxiong@whu.edu.cn.
Lijuan GuCentral Laboratory, Renmin Hospital of Wuhan University, Wuhan, 430060, China. gulijuan@whu.edu.cn.
Renmin Hospital of Wuhan University · CNWuhan University · CN

Funding

National Natural Science Foundation of China 81870939National Natural Science Foundation of China 81901994National Natural Science Foundation of China 82071339,81771283Natural Science Foundation of Hubei Province 2019CFB498
6 · The paper itself

Abstract

The nucleotide-binding oligomerization domain (NOD)-like receptor (NLR) family pyrin domain-containing 3 (NLRP3) inflammasome is a member of the NLR family of inherent immune cell sensors. The NLRP3 inflammasome can detect tissue damage and pathogen invasion through innate immune cell sensor components commonly known as pattern recognition receptors (PRRs). PRRs promote activation of nuclear factor kappa B (NF-κB) pathways and the mitogen-activated protein kinase (MAPK) pathway, thus increasing the transcription of genes encoding proteins related to the NLRP3 inflammasome. The NLRP3 inflammasome is a complex with multiple components, including an NAIP, CIITA, HET-E, and TP1 (NACHT) domain; apoptosis-associated speck-like protein containing a CARD (ASC); and a leucine-rich repeat (LRR) domain. After ischemic stroke, the NLRP3 inflammasome can produce numerous proinflammatory cytokines, mediating nerve cell dysfunction and brain edema and ultimately leading to nerve cell death once activated. Ischemic stroke is a disease with high rates of mortality and disability worldwide and is being observed in increasingly younger populations. To date, there are no clearly effective therapeutic strategies for the clinical treatment of ischemic stroke. Understanding the NLRP3 inflammasome may provide novel ideas and approaches because targeting of upstream and downstream molecules in the NLRP3 pathway shows promise for ischemic stroke therapy. In this manuscript, we summarize the existing evidence regarding the composition and activation of the NLRP3 inflammasome, the molecules involved in inflammatory pathways, and corresponding drugs or molecules that exert effects after cerebral ischemia. This evidence may provide possible targets or new strategies for ischemic stroke therapy.

Indexed as

AnimalsBrainCOVID-19HumansInflammasomesInflammationIschemic StrokeNLR Family, Pyrin Domain-Containing 3 ProteinInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinInflammationIschemic strokeNLRP3 inflammasomeReactive oxygen speciesSignaling pathway

Identifiers

PMID34059091
PMCPMC8166383
OpenAlexW3165628350

What OpenQuestion holds

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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.