Evidence map›Paper›PMID 40826276›Full record

ReviewNature immunology2025

The expanding role of the NLRP3 inflammasome from periodic fevers to therapeutic targets.

Alexander N R Weber, Róisín M McManus, Veit Hornung, Matthias Geyer, Jasmin B Kuemmerle-Deschner, Eicke Latz

Abstract readReview
PubMed Publisher
In one paragraph

Review in Nature immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Review
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  9. A century of cell death research.Journal of cell science · 2026
    Review
  10. Review
  11. 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
  12. Review
  13. Article
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  19. Review
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

6 authors.

Alexander N R WeberInstitute of Immunology, Department of Innate Immunity, University of Tübingen, Tübingen, Germany. alexander.weber@uni-tuebingen.de.ORCID http://orcid.org/0000-0002-8627-7056
Róisín M McManusGerman Center for Neurodegenerative Diseases (DZNE), Bonn, Germany.ORCID http://orcid.org/0000-0002-6896-0302
Veit HornungGene Center and Department of Biochemistry, Ludwig-Maximilians-Universität München, Munich, Germany.ORCID http://orcid.org/0000-0002-4150-194X
Matthias GeyerInstitute of Structural Biology, University of Bonn, Bonn, Germany.ORCID http://orcid.org/0000-0002-7718-5002
Jasmin B Kuemmerle-DeschnerDivision of Pediatric Rheumatology and Autoinflammation Reference Center Tübingen, Department of Pediatrics I, University Hospital Tübingen, Tübingen, Germany.
Eicke LatzDeutsches Rheuma-Forschungszentrum Berlin, Berlin, Germany. eicke.latz@drfz.de.ORCID http://orcid.org/0000-0003-1488-5666

Funding

Deutsche Forschungsgemeinschaft (German Research Foundation) EXC2124Deutsche Forschungsgemeinschaft (German Research Foundation) EXC2151Deutsche Forschungsgemeinschaft (German Research Foundation) EXC2180
6 · The paper itself

Abstract

Understanding and treating inflammation has proven a formidable challenge. The initiator and central motor of inflammation, the protein NLRP3, is an innate immune sentinel and nonspecific sensor of cellular perturbation. A wide array of inflammatory triggers prompts the formation of an NLRP3 'inflammasome' complex, leading to inflammatory interleukin-1 family cytokine release and pyroptotic cell death. Since gain-of-function mutations in NLRP3 were demonstrated to cause a rare autoinflammatory disease termed cryopyrin-associated periodic syndrome, NLRP3 has emerged as key mediator of inflammation in mouse models for many common diseases, including atherosclerosis, Alzheimer's disease and gout. But even though small-molecule NLRP3 modulators have entered clinical development, many aspects of NLRP3 activation and regulation in humans remain relatively unclear. This Review summarizes the current understanding of the molecular mechanisms that drive NLRP3 inflammasome activation and regulation, and discusses emerging targeting strategies. Understanding these processes can guide precision medicine approaches aimed at mitigating NLRP3-driven pathologies.

Indexed as

Cryopyrin-Associated Periodic SyndromesInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinAnimalsHumansInflammationMiceInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, human

Identifiers

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.