Component

GSDMD

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

2 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

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. Inflammatory caspase activation cleaves GSDMD to produce its cytotoxic N-terminal fragment in the inspected pyroptosis pathway.

    inflammatory caspases → cleaved GSDMD N-terminal fragment source_derived_draftliterature_reviewed:direct_experimental
    Experimental context and source evidence
    cell_type
    Macrophages
    experimental_model
    Myeloid Gpx4 models, macrophage cytosolic LPS/E. coli and mouse sepsis
    limitations
    Not a demonstrated complete human dietary-deficiency sequence.
    organism
    Mus musculus

    Selenium: literature corrections and mechanism additions · lines 1384–1394

    Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually · supports · Myeloid Gpx4 models, macrophage cytosolic LPS/E. coli and mouse sepsis · secondary_verified · secondary_verified

    ## caspase-gsdmd Caspases cut gasdermin before its execution fragment acts. Inflammatory caspase activation cleaves GSDMD to produce its cytotoxic N-terminal fragment in the inspected pyroptosis pathway. Organism: Mus musculus Cell type: Macrophages Experimental model: Myeloid Gpx4 models, macrophage cytosolic LPS/E. coli and mouse sepsis Limitations: Not a demonstrated complete human dietary-deficiency sequence. Primary reference: [Lipid peroxidation drives gasdermin D-mediated pyroptosis in lethal polymicrobial sepsis](https://pmc.ncbi.nlm.nih.gov/articles/PMC6043361/)
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards