Evidence map›Paper›PMID 25625584›Full record

ReviewRedox biology2015

NLRP3 inflammasome: from a danger signal sensor to a regulatory node of oxidative stress and inflammatory diseases.

Amna Abderrazak, Tatiana Syrovets, Dominique Couchie, Khadija El Hadri, Bertrand Friguet, Thomas Simmet, Mustapha Rouis

Open access · goldAbstract readReview
In one paragraph

Review in Redox biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 367 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
367citing papers in PubMed, 3 pooled it
25.0field-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

367 citing papers in PubMed, 3 syntheses or guidelines pooled it, 723 citations in OpenAlex.

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  10. King Oyster Mushroom,Nutrients · 2026
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307 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

7 authors at 3 institutions in 2 countries.

Amna AbderrazakSorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France; CNRS-UMR 8256, F-75005 Paris, France; Inserm U1164, F-75005 Paris, France.
Tatiana SyrovetsInstitute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, D-89081 Ulm, Germany.
Dominique CouchieSorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France; CNRS-UMR 8256, F-75005 Paris, France; Inserm U1164, F-75005 Paris, France.
Khadija El HadriSorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France; CNRS-UMR 8256, F-75005 Paris, France; Inserm U1164, F-75005 Paris, France.
Bertrand FriguetSorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France; CNRS-UMR 8256, F-75005 Paris, France; Inserm U1164, F-75005 Paris, France.
Thomas SimmetInstitute of Pharmacology of Natural Products & Clinical Pharmacology, Ulm University, D-89081 Ulm, Germany.
Mustapha RouisSorbonne Universités, UPMC Univ Paris 06, UMR 8256, Biological Adaptation and Ageing - IBPS, F-75005 Paris, France; CNRS-UMR 8256, F-75005 Paris, France; Inserm U1164, F-75005 Paris, France. Electronic address: mustapha.rouis@upmc.fr.
Inserm · FRAdaptation Biologique et VieillissementUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

IL-1β production is critically regulated by cytosolic molecular complexes, termed inflammasomes. Different inflammasome complexes have been described to date. While all inflammasomes recognize certain pathogens, it is the distinctive feature of NLRP3 inflammasome to be activated by many and diverse stimuli making NLRP3 the most versatile, and importantly also the most clinically implicated inflammasome. However, NLRP3 activation has remained the most enigmatic. It is not plausible that the intracellular NLRP3 receptor is able to detect all of its many and diverse triggers through direct interactions; instead, it is discussed that NLRP3 is responding to certain generic cellular stress-signals induced by the multitude of molecules that trigger its activation. An ever increasing number of studies link the sensing of cellular stress signals to a direct pathophysiological role of NLRP3 activation in a wide range of autoinflammatory and autoimmune disorders, and thus provide a novel mechanistic rational, on how molecules trigger and support sterile inflammatory diseases. A vast interest has created to unravel how NLRP3 becomes activated, since mechanistic insight is the prerequisite for a knowledge-based development of therapeutic intervention strategies that specifically target the NLRP3 triggered IL-1β production. In this review, we have updated knowledge on NLRP3 inflammasome assembly and activation and on the pyrin domain in NLRP3 that could represent a drug target to treat sterile inflammatory diseases. We have reported mutations in NLRP3 that were found to be associated with certain diseases. In addition, we have reviewed the functional link between NLRP3 inflammasome, the regulator of cellular redox status Trx/TXNIP complex, endoplasmic reticulum stress and the pathogenesis of diseases such as type 2 diabetes. Finally, we have provided data on NLRP3 inflammasome, as a critical regulator involved in the pathogenesis of obesity and cardiovascular diseases.

Indexed as

AnimalsCardiovascular DiseasesCarrier ProteinsDiabetes Mellitus, Type 2Gene Expression RegulationHumansInflammasomesInflammationInterleukin-18Interleukin-1betaMutationNLR Family, Pyrin Domain-Containing 3 ProteinObesityOxidative StressProtein Structure, TertiarySignal TransductionCarrier ProteinsInflammasomesInterleukin-18Interleukin-1betaNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanTXNIP protein, humanCardiovascular diseasesIL-18 (PDB id: Q14116)IL-1β (PDB id: P01584, P10749)NLRP3 inflammasome (PDB id: Q96P20)Obesity

Identifiers

PMID25625584
PMCPMC4315937
OpenAlexW2014054401

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.