ReviewFrontiers in immunology2026
Deciphering the NEK7-NLRP3 inflammasome assembly: from conformational activation to allosteric drug discovery.
Review in Frontiers in immunology, 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
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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.
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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.
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Who cites it
2 citing papers in PubMed.
- Pyroptosis in chronic obstructive pulmonary disease: Beyond the canonical NLRP3/Caspase-1/GSDMD pathway.Immunologic research · 2026Review
- From Xenobiotic Exposure to Neuroinflammation: Mechanisms Linking Lipopolysaccharide Signaling to Depressive-like Behavior.Journal of xenobiotics · 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NLRP3 inflammasome, a pivotal component of innate immunity, orchestrates immune defense and inflammatory responses. NEK7, an essential upstream regulator, drives inflammasome assembly through direct interaction with NLRP3. This review systematically summarizes the molecular mechanisms, upstream regulatory networks, and therapeutic targeting of the NEK7-NLRP3 axis. Structurally, NEK7 binds to the leucine-rich repeat (LRR) domain of NLRP3 via its catalytic domain, inducing conformational rearrangement and oligomerization. This structural shift exposes NLRP3's PYRIN domain (PYD), enabling ASC recruitment through homotypic PYD-PYD interactions and subsequent pro-caspase-1 activation to form the mature inflammasome complex. At the regulatory level, cell cycle-dependent NEK7 availability, post-translational modifications (phosphorylation/ubiquitination/palmitoylation), and numerous upstream signals-including kinases, ubiquitin ligases, ionic fluxes, miRNAs, and pathogens-collectively fine-tune the NEK7-NLRP3 interaction. In terms of therapeutic targeting, natural compounds from traditional Chinese medicine (e.g., oridonin, pristimerin), synthetic inhibitors (e.g., MCC950, entrectinib), and biological agents have been shown to suppress inflammasome activation by disrupting the NEK7-NLRP3 interface or modulating associated regulatory pathways. These advances offer novel therapeutic strategies for NLRP3-driven pathologies including gouty arthritis, ischemia-reperfusion injury, neurodegenerative disorders, and metabolic syndromes.
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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.