Component
Hepcidin expression
Hepcidin expression. Species, exposure and limitations are retained in each linked claim.
3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
BMP6 increased hepcidin expression and reduced serum iron in mice.
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 evidenceErythroferrone mediated hepcidin suppression during stress erythropoiesis.
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 evidenceIL-6 induced hepcidin in the tested human liver-cell, mouse and volunteer systems.
Experimental context and source evidence
- availability_state
- biomarker_context Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"}
- experimental_model
- Human liver-cell, mouse and human-volunteer inflammation experiments
- exposure
- IL-6 and inflammatory stimulation
- limitations
- IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway.
- nutrient_topic
- Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
- organism
- Humans and mice
- plain_language
- Inflammation can turn up the hormone that restricts iron release.
- primary_references
- [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945
- tissue_or_cell_type
- Liver and circulation
- trigger_kind
- biomarker_context Imported condition classification; unverified.
Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 875–886
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human liver-cell, mouse and human-volunteer inflammation experiments · source_derived_draft · unverified_draft
### iron-il6-hepcidin IL-6 induced hepcidin in the tested human liver-cell, mouse and volunteer systems. Condition category: biomarker_context nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inflammation can turn up the hormone that restricts iron release. organism: Humans and mice tissue_or_cell_type: Liver and circulation experimental_model: Human liver-cell, mouse and human-volunteer inflammation experiments limitations: IL-6 dependence applies to the tested inflammatory models, not every possible inflammatory iron pathway. exposure: IL-6 and inflammatory stimulation evidence_span: {"source_cache": "artifacts/iron-research/15124018.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830", "start_char": 0, "end_char": 578, "text_sha256": "f2ed307ef57c255917685bb7bfb1f02f3a6481c732cc2ee41ad1f338e2a2a830"} [iron-p15124018] IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin. (2004). https://pubmed.ncbi.nlm.nih.gov/15124018/ DOI: 10.1172/jci20945
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.