Evidence map›Paper›PMID 35600078›Full record

ReviewFrontiers in molecular neuroscience2022

NLRP3 Inflammasome Activation: A Therapeutic Target for Cerebral Ischemia-Reperfusion Injury.

Lixia Wang, Wei Ren, Qingjuan Wu, Tianzhu Liu, Ying Wei, Jiru Ding, Chen Zhou, Houping Xu, Sijin Yang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed, 1 pooled it
7.2field-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

67 citing papers in PubMed, 1 synthesis or guideline pooled it, 88 citations in OpenAlex.

  1. Pooled it
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  18. Gallic Acid Alleviates Cerebral Ischemia-reperfusion Injury in Mice by Mediating Microglial Polarization Through the NLRP3/mTOR Axis.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
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7 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

9 authors at 2 institutions in 1 country.

Lixia WangHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Wei RenThe Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
Qingjuan WuGuang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Tianzhu LiuThe Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
Ying WeiHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Jiru DingHospital of Chengdu University of Traditional Chinese Medicine, Chengdu, China.
Chen ZhouThe Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
Houping XuPreventive Treatment Center, The Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
Sijin YangThe Affiliated Traditional Chinese Medicine Hospital of Southwest Medical University, Luzhou, China.
Southwest Medical University · CNGuang’anmen Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Millions of patients are suffering from ischemic stroke, it is urgent to figure out the pathogenesis of cerebral ischemia-reperfusion (I/R) injury in order to find an effective cure. After I/R injury, pro-inflammatory cytokines especially interleukin-1β (IL-1β) upregulates in ischemic brain cells, such as microglia and neuron. To ameliorate the inflammation after cerebral I/R injury, nucleotide-binding oligomerization domain (NOD), leucine-rich repeat (LRR), and pyrin domain-containing protein 3 (NLRP3) inflammasome is well-investigated. NLRP3 inflammasomes are complicated protein complexes that are activated by endogenous and exogenous danger signals to participate in the inflammatory response. The assembly and activation of the NLRP3 inflammasome lead to the caspase-1-dependent release of pro-inflammatory cytokines, such as interleukin (IL)-1β and IL-18. Furthermore, pyroptosis is a pro-inflammatory cell death that occurs in a dependent manner on NLRP3 inflammasomes after cerebral I/R injury. In this review, we summarized the assembly and activation of NLRP3 inflammasome; moreover, we also concluded the pivotal role of NLRP3 inflammasome and inhibitors, targeting the NLRP3 inflammasome in cerebral I/R injury.

Indexed as

cerebral I/R injuryischemic strokemitochondrionNLRP3 inflammasome activationpyroptosis

Identifiers

PMID35600078
PMCPMC9122020
OpenAlexW4229041839

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.