Evidence map›Paper›PMID 23318584›Full record

ArticleCell research2013

Nitric oxide suppresses NLRP3 inflammasome activation and protects against LPS-induced septic shock.

Kairui Mao, Shuzhen Chen, Mingkuan Chen, Yonglei Ma, Yan Wang, Bo Huang, Zhengyu He, Yan Zeng, Yu Hu, Shuhui Sun and 7 more

Open access · hybridAbstract read
In one paragraph

Article in Cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
210citing papers in PubMed, 1 pooled it
13.5field-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

210 citing papers in PubMed, 1 synthesis or guideline pooled it, 393 citations in OpenAlex.

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  3. The role of NLRP3 inflammasome in 5-fluorouracil resistance of oral squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2017
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150 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors at 8 institutions in 2 countries.

Kairui MaoState Key Laboratory of Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Shuzhen Chen
Mingkuan Chen
Yonglei Ma
Yan Wang
Bo Huang
Zhengyu He
Yan Zeng
Yu Hu
Shuhui Sun
Jing Li
Xiaodong Wu
Xiangrui Wang
Warren Strober
Chang Chen
Guangxun Meng
Bing Sun
Institut Pasteur of Shanghai · CNChinese Academy of Sciences · CNShanghai Institutes for Biological Sciences · CNRenji Hospital · CNCenter for Excellence in Molecular Cell Science · CNCenter for Life Sciences · CNFudan University · CNNational Institutes of Health · US

Funding

Regulation Of Immune Responses In Humans and in Experimental AnimalsZIAAI000432 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$11.3M
Regulation of T cell DifferentiationZIAAI000872 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$9.6M
Immunoregulatory Defects In Inflammatory Bowel DiseaseZIAAI000354 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI STROBER, WARREN · 2009 to 2025
$8.7M
6 · The paper itself

Abstract

Inflammasomes are multi-protein complexes that trigger the activation of caspase-1 and the maturation of interleukin-1β (IL-1β), yet the regulation of these complexes remains poorly characterized. Here we show that nitric oxide (NO) inhibited the NLRP3-mediated ASC pyroptosome formation, caspase-1 activation and IL-1β secretion in myeloid cells from both mice and humans. Meanwhile, endogenous NO derived from iNOS (inducible form of NO synthase) also negatively regulated NLRP3 inflammasome activation. Depletion of iNOS resulted in increased accumulation of dysfunctional mitochondria in response to LPS and ATP, which was responsible for the increased IL-1β production and caspase-1 activation. iNOS deficiency or pharmacological inhibition of NO production enhanced NLRP3-dependent cytokine production in vivo, thus increasing mortality from LPS-induced sepsis in mice, which was prevented by NLRP3 deficiency. Our results thus identify NO as a critical negative regulator of the NLRP3 inflammasome via the stabilization of mitochondria. This study has important implications for the design of new strategies to control NLRP3-related diseases.

Indexed as

AnimalsCarrier ProteinsCaspase 1Cells, CulturedEnzyme ActivationHumansInflammasomesInterleukin-1betaLipopolysaccharidesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMitochondriaNitric OxideNitric Oxide Synthase Type IICarrier ProteinsCaspase 1InflammasomesInterleukin-1betaLipopolysaccharidesNitric OxideNitric Oxide Synthase Type IINLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mouseRNA, Small Interfering

Identifiers

PMID23318584
PMCPMC3567828
OpenAlexW2124178650

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.