Component

NLRP3

Independent entity for contextual scientific-audit claims; no universal nutritional effect implied.

8 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. TXNIP contributes to NLRP3 activation in the metabolic/oxidative-stress settings tested by Zhou and colleagues.

    TXNIP → NLRP3 source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    Studied metabolic/inflammatory cells
    experimental_model
    Cellular and mouse metabolic/oxidative-stress models
    limitations
    Other macrophage settings show Txnip-independent IL-1beta production.
    organism
    Mus musculus and cell models

    Selenium: literature corrections and mechanism additions · lines 1360–1370

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Cellular and mouse metabolic/oxidative-stress models · secondary_verified · secondary_verified

    ## txnip-nlrp3 TXNIP can help activate this inflammatory pathway in particular settings. TXNIP contributes to NLRP3 activation in the metabolic/oxidative-stress settings tested by Zhou and colleagues. Organism: Mus musculus and cell models Cell type: Studied metabolic/inflammatory cells Experimental model: Cellular and mouse metabolic/oxidative-stress models Limitations: Other macrophage settings show Txnip-independent IL-1beta production. Primary reference: [Thioredoxin-interacting protein links oxidative stress to inflammasome activation](https://pubmed.ncbi.nlm.nih.gov/20023662/)
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cucurbitacin B exposure was associated with the TLR4/mitochondrial-ROS/NLRP3 route and gasdermin D cleavage in the NSCLC pyroptosis experiments.

    Cucurbitacin B → Human NSCLC pyroptotic response during cucurbitacin B exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human NSCLC cells; mouse tumor experiments provide a separate translational level.
    limitations
    Do not merge all tumor-cell death into one obligatory linear chain.
    nutrient_topic
    Cucurbitacins collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Cucurbitacins
    plain_language
    Inflammatory membrane rupture is separate from ferroptotic lipid damage.
    primary_references
    Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748

    Cucurbitacins: thiol chemistry, cytoskeleton, metabolic dependencies and signaling (2026-09-20) · lines 300–306

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human NSCLC cells; mouse tumor experiments provide a separate translational level. · source_derived_draft · unverified_draft

    ## cucurbitacin-b-pyroptosis-route Inflammatory membrane rupture is separate from ferroptotic lipid damage. Cucurbitacin B exposure was associated with the TLR4/mitochondrial-ROS/NLRP3 route and gasdermin D cleavage in the NSCLC pyroptosis experiments. Model: Human NSCLC cells; mouse tumor experiments provide a separate translational level. Limitations: Do not merge all tumor-cell death into one obligatory linear chain. Evidence access: Primary abstract Cucurbitacin B inhibits non-small cell lung cancer in vivo and in vitro by triggering TLR4/NLRP3/GSDMD-dependent pyroptosis. · 2021 · https://pubmed.ncbi.nlm.nih.gov/34217831/ · DOI 10.1016/j.phrs.2021.105748
    Complete structured claim and evidence

  2. NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction.

    NIMA-related kinase 7 / NEK7 → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays.
    limitations
    NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Potassium loss signals through an assembly protein before caspase activation.
    primary_references
    [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    tissue_or_cell_type
    Bone-marrow macrophages

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 880–889

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. · source_derived_draft · unverified_draft

    ### k-efflux-nek7-assembly NEK7 loss blocked inflammasome assembly downstream of preserved K efflux; 50 mM KCl prevented the induced NEK7-NLRP3 interaction. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Potassium loss signals through an assembly protein before caspase activation. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Mouse macrophages with Nek7 deletion/reconstitution; ATP, nigericin or gramicidin; high-K control, interaction assays. limitations: NEK7 catalytic activity was dispensable; this is not proof of potassium binding directly to NEK7. [he-2016-nek7] NEK7 is an essential mediator of NLRP3 activation downstream of potassium efflux (2016). https://pmc.ncbi.nlm.nih.gov/articles/PMC4810788/ DOI: 10.1038/nature16959
    Complete structured claim and evidence

  3. Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles.

    Extracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Primed mouse macrophages, extracellular-K titration.
    exposure
    Artificial extracellular potassium elevation; not dietary excess.
    limitations
    Stimulus-specific; does not justify elevating blood potassium.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Reducing the outward potassium gradient blocked these activation routes.
    primary_references
    [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    tissue_or_cell_type
    Bone-marrow macrophages

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 868–878

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primed mouse macrophages, extracellular-K titration. · source_derived_draft · unverified_draft

    ### k-high-medium-nlrp3-block Raising extracellular K to 45 mM maximally inhibited NLRP3 responses to the tested toxins and particles. Condition category: normal nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing the outward potassium gradient blocked these activation routes. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: Primed mouse macrophages, extracellular-K titration. limitations: Stimulus-specific; does not justify elevating blood potassium. exposure: Artificial extracellular potassium elevation; not dietary excess. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    Complete structured claim and evidence

  4. K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss.

    Intracellular potassium concentration → NLRP3 inflammasome source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes.
    limitations
    Artificial cellular depletion; not a blood threshold or dietary inflammation experiment.
    nutrient_topic
    Potassium research collection; topical membership is not evidence of a direct dietary effect. · Potassium
    organism
    Mouse
    plain_language
    Experimentally losing cellular potassium could trigger this immune sensor.
    primary_references
    [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    tissue_or_cell_type
    Bone-marrow macrophages
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Potassium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 857–866

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. · source_derived_draft · unverified_draft

    ### k-macrophage-loss-nlrp3 K-free medium triggered NLRP3-dependent IL-1beta release in primed macrophages, accompanying intracellular K loss. Condition category: nutrient_deficiency nutrient_topic: Potassium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Experimentally losing cellular potassium could trigger this immune sensor. organism: Mouse tissue_or_cell_type: Bone-marrow macrophages experimental_model: LPS-primed mouse macrophages, 0 versus 5 mM K; response by 30 minutes. limitations: Artificial cellular depletion; not a blood threshold or dietary inflammation experiment. [munoz-2013-nlrp3] K+ efflux is the Common Trigger of NLRP3 inflammasome Activation by Bacterial Toxins and Particulate Matter (2013). https://pmc.ncbi.nlm.nih.gov/articles/PMC3730833/ DOI: 10.1016/j.immuni.2013.05.016
    Complete structured claim and evidence

  5. Adding 1 mM ergothioneine for 24 hours reduced IL-18 production in placental explants from women with gestational diabetes.

    L-Ergothioneine → Human interleukin 18 / IL18 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human placental explants; comparison with NLRP3 inhibitor MCC950.
    limitations
    Ex vivo result, not a pregnancy intervention trial or proof of direct NLRP3 binding.
    nutrient_topic
    Ergothioneine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Ergothioneine
    plain_language
    Inflammatory output fell in tissue studied outside the body.
    primary_references
    L-ergothioneine reduces mitochondrial-driven NLRP3 activation in gestational diabetes mellitus. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38029485/ · DOI 10.1016/j.jri.2023.104171

    Ergothioneine: transport, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 376–382

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human placental explants; comparison with NLRP3 inhibitor MCC950. · source_derived_draft · unverified_draft

    ## ergothioneine-placenta-il18 Inflammatory output fell in tissue studied outside the body. Adding 1 mM ergothioneine for 24 hours reduced IL-18 production in placental explants from women with gestational diabetes. Model: Human placental explants; comparison with NLRP3 inhibitor MCC950. Limitations: Ex vivo result, not a pregnancy intervention trial or proof of direct NLRP3 binding. Evidence access: Primary abstract L-ergothioneine reduces mitochondrial-driven NLRP3 activation in gestational diabetes mellitus. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38029485/ · DOI 10.1016/j.jri.2023.104171
    Complete structured claim and evidence

  6. Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin.

    Dihydrocapsaicin → The cGAS-STING pathway source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"}
    experimental_model
    Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation
    exposure
    Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation
    limitations
    The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence.
    nutrient_topic
    Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. · Dihydrocapsaicin
    organism
    Rat
    plain_language
    It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes.
    primary_references
    [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
    tissue_or_cell_type
    Skin flap vasculature

    Dihydrocapsaicin: the second capsaicinoid, the hypothermia it is used to induce, what the gut and liver do to it, and what it does without TRPV1 (2026-09-21) · lines 699–710

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation · source_derived_draft · unverified_draft

    ### dhc-suppresses-sting Dihydrocapsaicin enhanced the survival of multizone perforator flaps by suppressing the cGAS-STING pathway, oxidative stress and formation of the NLRP3 inflammasome, inducing oxidative stress resistance and preventing apoptosis in vascular endothelial cells, whereas activation of the cGAS-STING pathway led to accumulation of reactive oxygen species and NLRP3 inflammasome and diminished the protective role of dihydrocapsaicin. Condition category: normal nutrient_topic: Dihydrocapsaicin research collection; topical membership is not evidence of a direct clinical effect, and dihydrocapsaicin is recorded separately from capsaicin. plain_language: It protects starved tissue by switching off an inflammatory alarm; turn the alarm back on and the protection goes. organism: Rat tissue_or_cell_type: Skin flap vasculature experimental_model: Rat multizone perforator flap ischaemia-reperfusion model with network pharmacology prediction and pathway manipulation limitations: The pathway-activation arm is the useful control: switching the pathway back on removed the benefit. Network pharmacology prediction is hypothesis generation, not evidence. exposure: Dihydrocapsaicin with cGAS-STING pathway activation as a test of mediation evidence_span: {"source_cache": "artifacts/dihydrocapsaicin-research/38459660.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf", "start_char": 0, "end_char": 1793, "text_sha256": "f1a586e910230094fc4d9c5c54d57fb7ccab56a5c6565737d15a38c16f0567cf"} [dhc-p38459660] Dihydrocapsaicin suppresses the STING-mediated accumulation of ROS and NLRP3 inflammasome and alleviates apoptosis after ischemia-reperfusion injury of perforator skin flap. (2024). https://pubmed.ncbi.nlm.nih.gov/38459660/ DOI: 10.1002/ptr.8167
    Complete structured claim and evidence

  7. BHB prevented potassium efflux in the tested NLRP3 activation experiments.

    D-(R)-beta-hydroxybutyrate → Macrophage potassium efflux source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Stimulated innate immune cells; both BHB enantiomers were active.
    limitations
    Not evidence that BHB corrects systemic potassium deficiency.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    A ketone altered an ion movement involved in inflammatory signaling.
    primary_references
    The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 368–374

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Stimulated innate immune cells; both BHB enantiomers were active. · source_derived_draft · unverified_draft

    ## fast-bhb-potassium A ketone altered an ion movement involved in inflammatory signaling. BHB prevented potassium efflux in the tested NLRP3 activation experiments. Model: Stimulated innate immune cells; both BHB enantiomers were active. Limitations: Not evidence that BHB corrects systemic potassium deficiency. Evidence access: Primary abstract The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome-mediated inflammatory disease. · 2015 · https://pubmed.ncbi.nlm.nih.gov/25686106/ · DOI 10.1038/nm.3804
    Complete structured claim and evidence

In the sources

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