Component

Systemic tissue iron overload

Systemic tissue iron overload. Species, exposure and limitations are retained in each linked claim.

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

What acts on it

  1. Bmp6-null mice had reduced hepcidin expression and tissue iron overload.

    Mouse bone morphogenetic protein 6 / Bmp6 → Systemic tissue iron overload source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/19252486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f51b7e3f2c0882e3da19cc1f55c13f742c4cd47ca3db21bcc40be6263af76f2b", "start_char": 0, "end_char": 1168, "text_sha256": "f51b7e3f2c0882e3da19cc1f55c13f742c4cd47ca3db21bcc40be6263af76f2b"}
    experimental_model
    Ligand binding, antibody treatment and knockout studies
    exposure
    BMP6, BMP6 antibody, soluble HJV and Bmp6 deletion
    limitations
    Mouse causal regulation; the role of other BMP ligands is not excluded.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Mice and biochemical HJV/BMP systems
    plain_language
    An iron-control defect can produce excess stores despite the element being essential.
    primary_references
    [iron-p19252486] BMP6 is a key endogenous regulator of hepcidin expression and iron metabolism. (2009). https://pubmed.ncbi.nlm.nih.gov/19252486/ DOI: 10.1038/ng.335
    tissue_or_cell_type
    Liver, blood and tissues
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 797–808

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ligand binding, antibody treatment and knockout studies · source_derived_draft · unverified_draft

    ### iron-bmp6-overload Bmp6-null mice had reduced hepcidin expression and tissue iron overload. Condition category: machinery_impairment nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: An iron-control defect can produce excess stores despite the element being essential. organism: Mice and biochemical HJV/BMP systems tissue_or_cell_type: Liver, blood and tissues experimental_model: Ligand binding, antibody treatment and knockout studies limitations: Mouse causal regulation; the role of other BMP ligands is not excluded. exposure: BMP6, BMP6 antibody, soluble HJV and Bmp6 deletion evidence_span: {"source_cache": "artifacts/iron-research/19252486.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f51b7e3f2c0882e3da19cc1f55c13f742c4cd47ca3db21bcc40be6263af76f2b", "start_char": 0, "end_char": 1168, "text_sha256": "f51b7e3f2c0882e3da19cc1f55c13f742c4cd47ca3db21bcc40be6263af76f2b"} [iron-p19252486] BMP6 is a key endogenous regulator of hepcidin expression and iron metabolism. (2009). https://pubmed.ncbi.nlm.nih.gov/19252486/ DOI: 10.1038/ng.335
    Complete structured claim and evidence

  2. A major HFE missense alteration was homozygous in 83% of 178 hereditary-hemochromatosis patients in the discovery cohort.

    Human homeostatic iron regulator / HFE → Systemic tissue iron overload source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/8696333.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "812dfc62980bb4a17920e9eb490a2d1abc529b468c0531ffd59011713a60a15a", "start_char": 0, "end_char": 921, "text_sha256": "812dfc62980bb4a17920e9eb490a2d1abc529b468c0531ffd59011713a60a15a"}
    experimental_model
    Linkage disequilibrium and human genetic association
    exposure
    HFE discovery and missense variants
    limitations
    Historical selected population; 83% is not penetrance or a current general-population risk estimate.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    178 hereditary-hemochromatosis patients in the reported cohort
    plain_language
    The body’s iron-control machinery can be defective even when dietary supply is ordinary.
    primary_references
    [iron-p8696333] A novel MHC class I-like gene is mutated in patients with hereditary haemochromatosis. (1996). https://pubmed.ncbi.nlm.nih.gov/8696333/ DOI: 10.1038/ng0896-399
    tissue_or_cell_type
    Genetic iron-overload phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 1213–1224

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Linkage disequilibrium and human genetic association · source_derived_draft · unverified_draft

    ### iron-hfe-association A major HFE missense alteration was homozygous in 83% of 178 hereditary-hemochromatosis patients in the discovery cohort. Condition category: machinery_impairment nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The body’s iron-control machinery can be defective even when dietary supply is ordinary. organism: 178 hereditary-hemochromatosis patients in the reported cohort tissue_or_cell_type: Genetic iron-overload phenotype experimental_model: Linkage disequilibrium and human genetic association limitations: Historical selected population; 83% is not penetrance or a current general-population risk estimate. exposure: HFE discovery and missense variants evidence_span: {"source_cache": "artifacts/iron-research/8696333.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "812dfc62980bb4a17920e9eb490a2d1abc529b468c0531ffd59011713a60a15a", "start_char": 0, "end_char": 921, "text_sha256": "812dfc62980bb4a17920e9eb490a2d1abc529b468c0531ffd59011713a60a15a"} [iron-p8696333] A novel MHC class I-like gene is mutated in patients with hereditary haemochromatosis. (1996). https://pubmed.ncbi.nlm.nih.gov/8696333/ DOI: 10.1038/ng0896-399
    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