Evidence map›Paper›PMID 32700178›Full record

ArticleInflammation2020

Toll-Like Receptor 9 Is Involved in NLRP3 Inflammasome Activation and IL-1β Production Through Monosodium Urate-Induced Mitochondrial DNA.

Seong-Kyu Kim, Ki-Yeun Park, Jung-Yoon Choe

Abstract read
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In one paragraph

Article in Inflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
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  3. [Menstrual blood-derived mesenchymal stem cell transplantation improves anti-fibrosis mechanisms in mouse models of alcoholic liver fibrosis].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2026
    Article
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  7. Understanding a Potential Role for the NLRP3 Inflammasome in Placenta-Mediated Pregnancy Complications.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025
    Review
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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

3 authors at 1 institution in 1 country.

Seong-Kyu KimDepartment of Internal Medicine, Division of Rheumatology, Catholic University of Daegu School of Medicine, Daegu, Republic of Korea. kimsk714@cu.ac.kr.ORCID http://orcid.org/0000-0002-7780-0167
Ki-Yeun ParkArthritis and Autoimmunity Research Center, Catholic University of Daegu, Daegu, Republic of Korea.
Jung-Yoon ChoeDepartment of Internal Medicine, Division of Rheumatology, Catholic University of Daegu School of Medicine, Daegu, Republic of Korea.
Daegu Catholic University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLR family pyrin domain-containing 3 (NLRP3) inflammasome is a cytoplasmic multimolecular complex that generates interleukin (IL)-1β and is considered a main pathogenic mechanism for uric acid-induced inflammation. Whether toll-like receptor 9 (TLR9) is responsible for uric acid-induced NLRP3 inflammasome activation remains unclear. Thus, the aim of this study was to identify the role of TLR9 in NLRP3 inflammasome activation through monosodium urate (MSU) crystal-induced mitochondrial DNA. RAW 264.7 cells treated with MSU crystals, CpG oligonucleotides (ODNs), or a combination of both were used to assess nuclear factor (NF)-κB signaling, NLRP3 inflammasome components such as NLRP3, ASC, and caspase-1, and IL-1β. Real-time polymerase chain reaction (RT-PCR), Western blotting, DNA fragmentation assay, mitochondrial DNA copy number assay, and immunofluorescence were used in the in vitro study. RAW 264.7 cells treated with CpG-ODN stimulated the activation of NF-κB signaling, the NLRP3 inflammasome components NLRP3, ASC, and caspase-1, and IL-1β gene and protein expression. DNA fragmentation assay showed that MSU crystals induced cellular apoptosis. Fragmented DNA prompted by MSU crystals induced TLR9 expression. RAW 264.7 cells treated with CpG-ODN or MSU crystals and both increased expression of mitochondrial DNA relative to nuclear DNA. CpG-ODN and MSU crystals augmented the activation of NLRP3 inflammasome components and IL-1β expression, which was significantly suppressed in RAW 264.7 cells transfected with TLR9 siRNA. This study suggests that TLR9 activated by MSU crystal-mediated mitochondrial DNA contributes to the activation of NLRP3 inflammasomes and IL-1β production.

Indexed as

AnimalsDNA FragmentationDNA, MitochondrialInflammasomesInflammationInterleukin-1betaMacrophagesMiceNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinOligodeoxyribonucleotidesRAW 264.7 CellsReactive Oxygen SpeciesSignal TransductionToll-Like Receptor 9Uric AcidCPG-oligonucleotideDNA, MitochondrialIL1B protein, mouseInflammasomesInterleukin-1betaNF-kappa BNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseOligodeoxyribonucleotidesReactive Oxygen SpeciesTlr9 protein, mouseToll-Like Receptor 9Uric Acidinterleukin-1βmonosodium urateNF-κBNLRP3 inflammasometoll-like receptor 9

Identifiers

PMID32700178
OpenAlexW3044680910

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.