Evidence map›Paper›PMID 30277570›Full record

ArticleClinical and experimental immunology2018

NLRP3 inflammasome activation contributes to the pathogenesis of rheumatoid arthritis.

C Guo, R Fu, S Wang, Y Huang, X Li, M Zhou, J Zhao, N Yang

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers.

0numbers the graph read from it
0cells of the map it votes in
166citing papers in PubMed
8.6field-weighted citation impact, top 1% 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

166 citing papers in PubMed, 281 citations in OpenAlex.

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  4. [Regulatory mechanisms of post-translational modifications in inflammasome signaling: a review].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026
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  7. A novel small molecule KMU-11361 attenuates rheumatoid arthritis by mechanistic inhibition of the TAK1-NF-κB-NLRP3 axis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  11. Frontiers in pharmacology · 2026
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106 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

8 authors at 4 institutions in 1 country.

C GuoDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
R FuDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
S WangDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
Y HuangDepartment of Pediatrics, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
X LiDepartment of Orthopedic Surgery, Second School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou, China.
M ZhouDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
J ZhaoDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
N YangDepartment of Rheumatology, First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China.
The First Affiliated Hospital, Sun Yat-sen University · CNSun Yat-sen University · CNGuangzhou University of Chinese Medicine · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nucleotide-binding, oligomerization domain (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) gene polymorphism was reported to be associated with susceptibility, disease activity or anti-tumour necrosis factor (TNF) treatment response in rheumatoid arthritis (RA). However, the roles of NLRP3 inflammasome in the development of RA have not yet been elucidated fully. The present study aimed to study the role of NLRP3 inflammasome in RA. NLRP3 inflammasome activation in synovial tissues from RA and osteoarthritis (OA) patients were assessed by Western blot. Active caspase-1 in synovia was stained by a FAM-FLICA caspase-1 probe. Mice with collagen-induced arthritis (CIA) were treated with MCC950, a selective NLRP3 inhibitor, or vehicle for 2 weeks. The clinical score of arthritis, synovial inflammation and cartilage erosion were assessed. Proinflammatory cytokines were measured by enzyme-linked immunosorbent assay (ELISA). The results showed that NLRP3 inflammasome was highly activated in both synovia from RA patients and CIA mice. Activation of NLRP3 inflammasome occurred mainly in the infiltrating monocyte/macrophages in synovia, but not in fibroblast-like synoviocytes. Treatment with MCC950 resulted in significantly less severe joints inflammation and bone destruction. NLRP3 inflammasome activation in the synovia was inhibited significantly by MCC950 with reduced production of interleukin (IL)-1β. The inhibition of NLRP3 inflammasome activation by MCC950 was confirmed further in a human monocytic cell line, THP-1. In conclusion, NLRP3 inflammasome is involved in the pathogenesis of RA. Targeting NLRP3 inflammasome with a small molecule inhibitor might be a novel therapeutic strategy for RA.

Indexed as

AnimalsArthritis, ExperimentalArthritis, RheumatoidCaspase 1CytokinesDisease Models, AnimalHumansInflammasomesInflammation MediatorsMaleMiceMice, Inbred DBANLR Family, Pyrin Domain-Containing 3 ProteinOsteoarthritisPolymorphism, GeneticSynovial MembraneCaspase 1CytokinesInflammasomesInflammation MediatorsNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 inflammasomeNLRP3 inhibitorrheumatoid arthritis

Identifiers

PMID30277570
PMCPMC6194337
OpenAlexW2891100999

What OpenQuestion holds

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Read underepoch 390

Registered trials

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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.