Evidence map›Paper›PMID 28779175›Full record

ArticleNature communications2017

CLICs-dependent chloride efflux is an essential and proximal upstream event for NLRP3 inflammasome activation.

Tiantian Tang, Xueting Lang, Congfei Xu, Xiaqiong Wang, Tao Gong, Yanqing Yang, Jun Cui, Li Bai, Jun Wang, Wei Jiang and 1 more

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

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 225 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
225citing papers in PubMed, 2 pooled it
9.3field-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

225 citing papers in PubMed, 2 syntheses or guidelines pooled it, 349 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Article
  5. Review
  6. Article
  7. Ciclopirox Olamine Inhibits the NLRP3 Inflammasome to Alleviate Inflammatory Diseases.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Review
  9. Article
  10. Article
  11. Rapid Proteome-Wide Discovery of Protein-Protein Interactions With ppIRIS.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  12. Targeting the polyene chain represents an adjuvant strategy for optimizing polyene antifungals.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  13. Review
  14. Review
  15. Review
  16. Molecular mechanisms of NLRP3 inflammasome activation.Experimental & molecular medicine · 2026
    Review
  17. Review
  18. Review
  19. Review
  20. Review

165 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

11 authors at 3 institutions in 1 country.

Tiantian TangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Xueting LangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Congfei XuInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Xiaqiong WangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Tao GongInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Yanqing YangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Jun CuiKey Laboratory of Gene Engineering of the Ministry of Education, State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, 510080, China.
Li BaiInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Jun WangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China.
Wei JiangInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China. ustcjw@ustc.edu.cn.
Rongbin ZhouInstitute of Immunology and the CAS Key Laboratory of Innate Immunity and Chronic Disease, CAS center for Excellence in Molecular Cell Sciences, School of Life Sciences and Medical Center, University of Science and Technology of China, Hefei, 230027, China. zrb1980@ustc.edu.cn.
University of Science and Technology of China · CNCenter for Excellence in Molecular Cell Science · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The NLRP3 inflammasome can sense different pathogens or danger signals, and has been reported to be involved in the development of many human diseases. Potassium efflux and mitochondrial damage are both reported to mediate NLRP3 inflammasome activation, but the underlying, orchestrating signaling events are still unclear. Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation. NLRP3 agonists induce potassium efflux, which causes mitochondrial damage and ROS production. Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1β secretion. Thus, our results identify CLICs-dependent chloride efflux as an essential and proximal upstream event for NLRP3 activation.The NLRP3 inflammasome is key to the regulation of innate immunity against pathogens or stress, but the underlying signaling regulation is still unclear. Here the authors show that chloride intracellular channels (CLIC) interface between mitochondria stress and inflammasome activation to modulate inflammatory responses.

Indexed as

AnimalsCell Line, TumorCells, CulturedChloride ChannelsChloridesHumansImmunoblottingInflammasomesIon TransportMice, Inbred C57BLMice, KnockoutMitochondriaMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinPotassiumProtein BindingChloride ChannelsChloridesClic1 protein, mouseCLIC5 protein, mouseCLIC protein, mouseInflammasomesMitochondrial ProteinsNLR Family, Pyrin Domain-Containing 3 ProteinNlrp3 protein, mousePotassiumReactive Oxygen Species

Identifiers

PMID28779175
PMCPMC5544706
OpenAlexW2740616875

What OpenQuestion holds

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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.