Component

Mouse hepcidin / Hamp

Mouse hepcidin / Hamp. Species, exposure and limitations are retained in each linked claim.

5 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. Hepatic hepcidin expression was suppressed.

    Curcumin → Mouse hepcidin / Hamp source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/curcumin-research/24634837.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7", "start_char": 0, "end_char": 1451, "text_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7"}
    experimental_model
    Six-month feeding comparison in C57BL/6J mice
    exposure
    Diet containing 0.2% curcumin versus unsupplemented diet
    limitations
    Long-term mouse findings cannot be equated with acute human supplementation. Expression changes may be adaptive responses, not direct target binding.
    nutrient_topic
    Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
    organism
    Mus musculus
    plain_language
    An iron-regulating signal fell in this mouse context.
    primary_references
    [curcumin-p24634837] Curcumin may impair iron status when fed to mice for six months. (2014). https://pubmed.ncbi.nlm.nih.gov/24634837/ DOI: 10.1016/j.redox.2014.01.018
    tissue_or_cell_type
    Liver and spleen

    Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 658–669

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-month feeding comparison in C57BL/6J mice · source_derived_draft · unverified_draft

    ### curcumin-mouse-hepcidin Hepatic hepcidin expression was suppressed. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: An iron-regulating signal fell in this mouse context. organism: Mus musculus tissue_or_cell_type: Liver and spleen experimental_model: Six-month feeding comparison in C57BL/6J mice limitations: Long-term mouse findings cannot be equated with acute human supplementation. Expression changes may be adaptive responses, not direct target binding. exposure: Diet containing 0.2% curcumin versus unsupplemented diet evidence_span: {"source_cache": "artifacts/curcumin-research/24634837.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7", "start_char": 0, "end_char": 1451, "text_sha256": "3c64f5d7dd7206fa30f155d11ee68a90c72432b6ff1837922ee17ef1e811fec7"} [curcumin-p24634837] Curcumin may impair iron status when fed to mice for six months. (2014). https://pubmed.ncbi.nlm.nih.gov/24634837/ DOI: 10.1016/j.redox.2014.01.018
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. BMP6 increased hepcidin expression and reduced serum iron in mice.

    Mouse bone morphogenetic protein 6 / Bmp6 → Hepcidin expression source_derived_draftungraded
    Experimental context and source evidence
    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
    This signaling pathway tells the body to restrict iron entry into the circulation.
    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

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 784–795

    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-hepcidin BMP6 increased hepcidin expression and reduced serum iron in mice. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: This signaling pathway tells the body to restrict iron entry into the circulation. 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. 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

  3. Erythroferrone mediated hepcidin suppression during stress erythropoiesis.

    Mouse erythroferrone / Erfe → Hepcidin expression source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/iron-research/24880340.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e290e3082fe90ef8ef538ec8d5151082e3d38672abfba19731ea158957fcc54", "start_char": 0, "end_char": 738, "text_sha256": "1e290e3082fe90ef8ef538ec8d5151082e3d38672abfba19731ea158957fcc54"}
    experimental_model
    Hemorrhage, erythropoietin response and gene deletion
    exposure
    Blood loss, EPO stimulation and Erfe deletion; thalassemia model
    limitations
    Stress erythropoiesis and mouse overload mechanisms; the author correction (PMID 32107478; https://doi.org/10.1038/s41588-019-0548-y) corrects swapped human FAM132B and HPRT primer labels in Supplementary Table 2.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Mice
    plain_language
    The request relaxes the hormone-controlled restriction on iron supply.
    primary_references
    [iron-p24880340] Identification of erythroferrone as an erythroid regulator of iron metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/24880340/ DOI: 10.1038/ng.2996
    tissue_or_cell_type
    Erythroblasts and hepatic iron regulation

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 823–834

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hemorrhage, erythropoietin response and gene deletion · source_derived_draft · unverified_draft

    ### iron-erfe-hepcidin Erythroferrone mediated hepcidin suppression during stress erythropoiesis. Condition category: normal nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The request relaxes the hormone-controlled restriction on iron supply. organism: Mice tissue_or_cell_type: Erythroblasts and hepatic iron regulation experimental_model: Hemorrhage, erythropoietin response and gene deletion limitations: Stress erythropoiesis and mouse overload mechanisms; the author correction (PMID 32107478; https://doi.org/10.1038/s41588-019-0548-y) corrects swapped human FAM132B and HPRT primer labels in Supplementary Table 2. exposure: Blood loss, EPO stimulation and Erfe deletion; thalassemia model evidence_span: {"source_cache": "artifacts/iron-research/24880340.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1e290e3082fe90ef8ef538ec8d5151082e3d38672abfba19731ea158957fcc54", "start_char": 0, "end_char": 738, "text_sha256": "1e290e3082fe90ef8ef538ec8d5151082e3d38672abfba19731ea158957fcc54"} [iron-p24880340] Identification of erythroferrone as an erythroid regulator of iron metabolism. (2014). https://pubmed.ncbi.nlm.nih.gov/24880340/ DOI: 10.1038/ng.2996
    Complete structured claim and evidence

  4. Intestinal Hif2a deletion lowered serum and liver iron and markedly reduced liver hepcidin expression.

    Mouse hypoxia-inducible factor 2 alpha / Epas1 → Serum iron concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/19352007.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040", "start_char": 0, "end_char": 1411, "text_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040"}
    experimental_model
    Conditional intestinal Hif1a/Hif2a knockout
    exposure
    Separate Hif1a versus Hif2a deletion
    limitations
    HIF isoforms were not interchangeable in this mouse experiment.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    Mice
    plain_language
    A hormonal attempt to increase iron availability did not replace the missing intestinal regulator.
    primary_references
    [iron-p19352007] HIF-2alpha, but not HIF-1alpha, promotes iron absorption in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19352007/ DOI: 10.1172/jci38499
    tissue_or_cell_type
    Duodenal epithelium and systemic iron
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 862–873

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional intestinal Hif1a/Hif2a knockout · source_derived_draft · unverified_draft

    ### iron-hif2-loss Intestinal Hif2a deletion lowered serum and liver iron and markedly reduced liver hepcidin expression. Condition category: machinery_impairment nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: A hormonal attempt to increase iron availability did not replace the missing intestinal regulator. organism: Mice tissue_or_cell_type: Duodenal epithelium and systemic iron experimental_model: Conditional intestinal Hif1a/Hif2a knockout limitations: HIF isoforms were not interchangeable in this mouse experiment. exposure: Separate Hif1a versus Hif2a deletion evidence_span: {"source_cache": "artifacts/iron-research/19352007.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040", "start_char": 0, "end_char": 1411, "text_sha256": "623fedcdd407c02879254b087510cff95b61336f7605c2430f51ab75ac550040"} [iron-p19352007] HIF-2alpha, but not HIF-1alpha, promotes iron absorption in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19352007/ DOI: 10.1172/jci38499
    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