Evidence map›Paper›PMID 33044555›Full record

ReviewThe Journal of cell biology2020

The NLRP3-inflammasome as a sensor of organelle dysfunction.

Paula I Seoane, Bali Lee, Christopher Hoyle, Shi Yu, Gloria Lopez-Castejon, Martin Lowe, David Brough

Open access · greenAbstract readReview
In one paragraph

Review in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed, 1 pooled it
6.3field-weighted citation impact, top 2% 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

104 citing papers in PubMed, 1 synthesis or guideline pooled it, 185 citations in OpenAlex.

  1. Pooled it
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  7. Whole-GrainMolecules (Basel, Switzerland) · 2026
    Article
  8. Review
  9. Article
  10. Diverse Scaffolds Facilitate NLRP3 Clustering and Inflammasome Formation in Response to Perturbations in Cell Homeostasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
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  12. Article
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44 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 1 institution in 1 country.

Paula I SeoaneDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Bali LeeDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Christopher HoyleDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Shi YuDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Gloria Lopez-CastejonDivision of Infection, Immunity, and Respiratory Medicine, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Martin LoweDivision of Molecular and Cellular Function, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
David BroughDivision of Neuroscience and Experimental Psychology, School of Biological Sciences, Faculty of Biology, Medicine, and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, UK.
Manchester Academic Health Science Centre · GB

Funding

Medical Research Council MR/T016515/1
6 · The paper itself

Abstract

Diverse pathogen- and damage-associated stresses drive inflammation via activation of the multimolecular NLRP3-inflammasome complex. How the effects of diverse stimuli are integrated by the cell to regulate NLRP3 has been the subject of intense research, and yet an accepted unifying hypothesis for the control of NLRP3 remains elusive. Here, we review the literature on the effects of NLRP3-activating stimuli on subcellular organelles and conclude that a shared feature of NLRP3-activating stresses is an organelle dysfunction. In particular, we propose that the endosome may be more important than previously recognized as a signal-integrating hub for NLRP3 activation in response to many stimuli and may also link to the dysfunction of other organelles. In addition, NLRP3-inflammasome-activating stimuli trigger diverse posttranslational modifications of NLRP3 that are important in controlling its activation. Future research should focus on how organelles respond to specific NLRP3-activating stimuli, and how this relates to posttranslational modifications, to delineate the organellar control of NLRP3.

Indexed as

Protein Processing, Post-TranslationalSignal TransductionStress, PhysiologicalAnimalsHumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinOrganellesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

PMID33044555
PMCPMC7543090
OpenAlexW3092041441

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.