Component

Mouse cathepsin B

Context-specific entity; species, compartment and exposure are stated on each claim.

4 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 it acts on

  1. Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study.

    Mouse cathepsin B → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse bone-marrow macrophages with silica/MSU comparisons.
    limitations
    Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Genetic loss did not reproduce the inhibitor-based necessity claim.
    primary_references
    Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 472–478

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse bone-marrow macrophages with silica/MSU comparisons. · source_derived_draft · unverified_draft

    ## silica-cathepsin-knockout Genetic loss did not reproduce the inhibitor-based necessity claim. Cathepsin-B-deficient macrophages retained crystal-induced IL-1 beta release in this study. Model: Mouse bone-marrow macrophages with silica/MSU comparisons. Limitations: Compensation and other cathepsins remain possible; no universal dismissal of lysosomal injury. Evidence access: Primary full text Activation of NLRP3 inflammasome by crystalline structures via cell surface contact. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25445147/ · DOI 10.1038/srep07281
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step.

    CA-074-Me treatment of silica-exposed mouse macrophages → Mouse IL-1 beta source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse macrophages; 10 micromolar CA-074-Me.
    limitations
    Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A lysosomal protease inhibitor reduced inflammatory output.
    primary_references
    Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 448–454

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophages; 10 micromolar CA-074-Me. · source_derived_draft · unverified_draft

    ## silica-cathepsin-inhibitor A lysosomal protease inhibitor reduced inflammatory output. CA-074-Me reduced silica-triggered IL-1 beta release, supporting a cathepsin-sensitive step. Model: Mouse macrophages; 10 micromolar CA-074-Me. Limitations: Pharmacology alone does not establish unique cathepsin B necessity. Correction record: A 2026 author correction replaces an erroneously duplicated lower-left Fig. 8c micrograph with the retrieved original. This is a figure correction, not a scientific contradiction or retraction. https://www.nature.com/articles/s41590-026-02468-9 Evidence access: Primary full text Silica crystals and aluminum salts activate the NALP3 inflammasome through phagosomal destabilization. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18604214/ · DOI 10.1038/ni.1631
    Complete structured claim and evidence

  2. Leupeptin reduced the measured cathepsin-B signal without preventing the nanoparticle-associated pyroptosis response.

    Leupeptin → Pyroptosis-associated response in mouse RAW-ASC cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse RAW-ASC cells; 1 microgram/mL leupeptin.
    limitations
    Leupeptin is not cathepsin-B-specific; measured abundance is not a selective genetic activity test.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    A protease-inhibitor result also failed to establish cathepsin B necessity.
    primary_references
    Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 512–518

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse RAW-ASC cells; 1 microgram/mL leupeptin. · source_derived_draft · unverified_draft

    ## silica-leupeptin-null A protease-inhibitor result also failed to establish cathepsin B necessity. Leupeptin reduced the measured cathepsin-B signal without preventing the nanoparticle-associated pyroptosis response. Model: Mouse RAW-ASC cells; 1 microgram/mL leupeptin. Limitations: Leupeptin is not cathepsin-B-specific; measured abundance is not a selective genetic activity test. Evidence access: Primary full text Characterization of Cathepsin B in Mediating Silica Nanoparticle-Induced Macrophage Pyroptosis via an NLRP3-Dependent Manner. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35966002/ · DOI 10.2147/JIR.S371536
    Complete structured claim and evidence

  3. MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake.

    Mouse MARCO → Lysosomal permeabilization in silica-exposed mouse macrophages source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Primary mouse macrophages; silica 100 micrograms/mL.
    limitations
    Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements.
    nutrient_topic
    Silica collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Silica and soluble silicon
    plain_language
    Less uptake did not necessarily mean less inflammation.
    primary_references
    Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Silica: soluble silicon, cellular transport and particle-specific mechanisms (2026-09-19) · lines 488–494

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Primary mouse macrophages; silica 100 micrograms/mL. · source_derived_draft · unverified_draft

    ## silica-marco-lysosome-loss Less uptake did not necessarily mean less inflammation. MARCO-null alveolar macrophages showed greater lysosomal leakage and IL-1 beta/caspase-1 responses despite lower silica uptake. Model: Primary mouse macrophages; silica 100 micrograms/mL. Limitations: Receptor uptake and lysosomal resilience are separate functions; not a contradiction of uptake measurements. Evidence access: Primary full text Role of lysosomes in silica-induced inflammasome activation and inflammation in absence of MARCO. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25054161/ · DOI 10.1155/2014/304180
    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