Evidence map›Paper›PMID 34053242›Full record

ReviewASN neuro

The Role of NLRP3 Inflammasome in Cerebrovascular Diseases Pathology and Possible Therapeutic Targets.

Rongrong Bai, Yue Lang, Jie Shao, Yu Deng, Reyisha Refuhati, Li Cui

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

Review in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
5.4field-weighted citation impact, top 3% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.

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  9. 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

6 authors at 1 institution in 1 country.

Rongrong BaiDepartment of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.ORCID 0000-0003-3454-0569
Yue LangDepartment of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Jie ShaoDepartment of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Yu DengDepartment of Hepatopancreatobiliary Surgery, The First Hospital of Jilin University, Changchun, China.
Reyisha RefuhatiDepartment of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Li CuiDepartment of Neurology, Neuroscience Center, The First Hospital of Jilin University, Changchun, China.
Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cerebrovascular diseases are pathological conditions involving impaired blood flow in the brain, primarily including ischaemic stroke, intracranial haemorrhage, and subarachnoid haemorrhage. The nucleotide-binding and oligomerisation (NOD) domain-like receptor (NLR) family pyrin domain (PYD)-containing 3 (NLRP3) inflammasome is a protein complex and a vital component of the immune system. Emerging evidence has indicated that the NLRP3 inflammasome plays an important role in cerebrovascular diseases. The function of the NLRP3 inflammasome in the pathogenesis of cerebrovascular diseases remains an interesting field of research. In this review, we first summarised the pathological mechanism of cerebrovascular diseases and the pathological mechanism of the NLRP3 inflammasome in aggravating atherosclerosis and cerebrovascular diseases. Second, we outlined signalling pathways through which the NLRP3 inflammasome participates in aggravating or mitigating cerebrovascular diseases. Reactive oxygen species (ROS)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ROS/thioredoxin-interacting protein (TXNIP) and purinergic receptor-7 (P2X7R) signalling pathways can activate the NLRP3 inflammasome; activation of the NLRP3 inflammasome can aggravate cerebrovascular diseases by mediating apoptosis and pyroptosis. Autophagy/mitochondrial autophagy, nuclear factor E2-related factor-2 (Nrf2), interferon (IFN)-β, sirtuin (SIRT), and phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) reportedly alleviate cerebrovascular diseases by inhibiting NLRP3 inflammasome activation. Finally, we explored specific inhibitors of the NLRP3 inflammasome based on the two-step activation of the NLRP3 inflammasome, which can be developed as new drugs to treat cerebrovascular diseases.

Indexed as

AnimalsCarrier ProteinsCerebrovascular DisordersDiterpenes, KauraneDrug Delivery SystemsFuransHumansIndenesNLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesReceptors, Purinergic P2X7SulfonamidesCarrier ProteinsDiterpenes, KauraneFuransIndenesN-(1,2,3,5,6,7-hexahydro-S-indacen-4-ylcarbamoyl)-4-(2-hydroxy-2-propanyl)-2-furansulfonamideNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanoridoninP2RX7 protein, humanReactive Oxygen SpeciesReceptors, Purinergic P2X7SulfonamidesTXNIP protein, humanatherosclerosisintracerebral haemorrhageischaemia strokeNLRP3 inflammasomesubarachnoid haemorrhage

Identifiers

PMID34053242
PMCPMC8168029
OpenAlexW3165218810

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.