ReviewCommunications biology2026
Sensing the spectrum: diverse stimuli for the NLRP3 inflammasome.
Review in Communications biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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.
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.
Who cites it
2 citing papers in PubMed.
- The NLRP3 inflammasome at the crossroads of innate immune signaling and cell death.Cellular & molecular immunology · 2026Review
- Tissue-Resident Macrophage in Inflammation and Cancer.MedComm · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The NLRP3 inflammasome is a central inflammatory signaling pathway in host defense, cancer, metabolic disorders, and neurodegenerative diseases. Unlike other pattern-recognition receptors, NLRP3 senses perturbations in organelle integrity and ion homeostasis, enabling its activation by a remarkably broad spectrum of pathogen-derived and cellular stress signals. In this review, we summarize recent advances that have expanded our understanding of the diverse classes of NLRP3 stimuli and highlight breakthroughs in elucidating the molecular mechanisms underlying both infection-driven and sterile inflammation. Finally, we discuss unresolved questions surrounding the physiological relevance of NLRP3 stimuli and the nature of uncharacterized stimuli in sterile inflammatory diseases, emphasizing how resolving these gaps may inform targeted therapeutic development.
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What OpenQuestion holds
Registered trials
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.