Component
Mouse heme oxygenase 1 / Hmox1
Mouse heme oxygenase 1 / Hmox1. Species, exposure and limitations are retained in each linked claim.
7 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 it acts on
HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse macrophage pharmacological and genetic comparisons.
- limitations
- The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- Removing HO-1 tested whether the observed effect needed that enzyme.
- primary_references
- Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 393–399
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage pharmacological and genetic comparisons. · source_derived_draft · unverified_draft
## taurine-ho1-required Removing HO-1 tested whether the observed effect needed that enzyme. HO-1 inhibition, knockdown or genetic absence blocked the enhancement of macrophage phagocytosis by taurine chloramine, while overexpression augmented it. Model: Mouse macrophage pharmacological and genetic comparisons. Limitations: The mechanism concerns this phagocytosis assay, not all actions of taurine chloramine. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidence
What acts on it
DIM increased HO-1 mRNA and protein in the mouse fibroblast study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/dim-research/21615272.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8", "start_char": 0, "end_char": 737, "text_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8"}
- experimental_model
- Reporter and gene/protein expression experiments
- exposure
- DIM compared with I3C and sulforaphane
- limitations
- Mouse cells; transcriptional induction does not establish clinical antioxidant benefit or nutrient repletion.
- nutrient_topic
- Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. · 3,3'-Diindolylmethane / DIM
- organism
- Mouse NIH3T3 fibroblasts
- plain_language
- This downstream enzyme is recorded separately from the Nrf2 regulator.
- primary_references
- [dim-p21615272] 3,3'-Diindolylmethane but not indole-3-carbinol activates Nrf2 and induces Nrf2 target gene expression in cultured murine fibroblasts. (2011). https://pubmed.ncbi.nlm.nih.gov/21615272/ DOI: 10.3109/10715762.2011.571683
- tissue_or_cell_type
- Nrf2-regulated defense genes
Diindolylmethane (DIM): formation, receptor signaling, metabolism and drug interactions (2026-09-17) · lines 1247–1258
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reporter and gene/protein expression experiments · source_derived_draft · unverified_draft
### dim-nrf2-mouse-hmox1 DIM increased HO-1 mRNA and protein in the mouse fibroblast study. Condition category: normal nutrient_topic: Diindolylmethane (DIM) research collection; topical membership is not evidence of a direct dietary effect. plain_language: This downstream enzyme is recorded separately from the Nrf2 regulator. organism: Mouse NIH3T3 fibroblasts tissue_or_cell_type: Nrf2-regulated defense genes experimental_model: Reporter and gene/protein expression experiments limitations: Mouse cells; transcriptional induction does not establish clinical antioxidant benefit or nutrient repletion. exposure: DIM compared with I3C and sulforaphane evidence_span: {"source_cache": "artifacts/dim-research/21615272.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8", "start_char": 0, "end_char": 737, "text_sha256": "1ae26f09db419c2cd095519c3326616a14343b52e23a71e7994a4aed764ab1b8"} [dim-p21615272] 3,3'-Diindolylmethane but not indole-3-carbinol activates Nrf2 and induces Nrf2 target gene expression in cultured murine fibroblasts. (2011). https://pubmed.ncbi.nlm.nih.gov/21615272/ DOI: 10.3109/10715762.2011.571683
Complete structured claim and evidenceTaurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Murine peritonitis, isolated macrophages and RAW264.7 cells.
- limitations
- This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron.
- nutrient_topic
- Taurine collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Taurine
- plain_language
- The derivative changed an enzyme involved in stress responses.
- primary_references
- Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Taurine: synthesis, transport, mitochondrial decoding and nutrient interactions (2026-09-19) · lines 385–391
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Murine peritonitis, isolated macrophages and RAW264.7 cells. · source_derived_draft · unverified_draft
## taurine-taucl-ho1 The derivative changed an enzyme involved in stress responses. Taurine chloramine treatment increased HO-1 expression in mouse peritoneal macrophages in the zymosan inflammation study. Model: Murine peritonitis, isolated macrophages and RAW264.7 cells. Limitations: This is a derivative and mouse immune-cell result, not evidence that taurine directly supplies or removes iron. Evidence access: Primary abstract Role of heme oxygenase-1 in potentiation of phagocytic activity of macrophages by taurine chloramine: Implications for the resolution of zymosan A-induced murine peritonitis. · 2018 · https://pubmed.ncbi.nlm.nih.gov/29477410/ · DOI 10.1016/j.cellimm.2018.02.003
Complete structured claim and evidenceCurcumin induced HO-1 expression in JB6 cells.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"}
- experimental_model
- Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays
- exposure
- Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct
- limitations
- Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement.
- nutrient_topic
- Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
- organism
- Mus musculus; transfected construct species not resolved in indexed abstract
- plain_language
- The stress-response pathway increased a heme-processing enzyme.
- primary_references
- [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
- tissue_or_cell_type
- JB6 epidermal cells and mouse skin
Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 372–383
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays · source_derived_draft · unverified_draft
### curcumin-ho1 Curcumin induced HO-1 expression in JB6 cells. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The stress-response pathway increased a heme-processing enzyme. organism: Mus musculus; transfected construct species not resolved in indexed abstract tissue_or_cell_type: JB6 epidermal cells and mouse skin experimental_model: Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays limitations: Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement. exposure: Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct evidence_span: {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"} [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
Complete structured claim and evidenceNrf2 siRNA abrogated curcumin-induced HO-1 expression.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"}
- experimental_model
- Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays
- exposure
- Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct
- limitations
- Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement.
- nutrient_topic
- Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
- organism
- Mus musculus; transfected construct species not resolved in indexed abstract
- plain_language
- This response required functioning Nrf2 machinery.
- primary_references
- [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
- tissue_or_cell_type
- JB6 epidermal cells and mouse skin
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 411–422
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays · source_derived_draft · unverified_draft
### curcumin-nrf2-loss Nrf2 siRNA abrogated curcumin-induced HO-1 expression. Condition category: machinery_impairment nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This response required functioning Nrf2 machinery. organism: Mus musculus; transfected construct species not resolved in indexed abstract tissue_or_cell_type: JB6 epidermal cells and mouse skin experimental_model: Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays limitations: Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement. exposure: Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct evidence_span: {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"} [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
Complete structured claim and evidenceTetrahydrocurcumin failed to reproduce HO-1 induction in this comparison.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"}
- experimental_model
- Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays
- exposure
- Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct
- limitations
- Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement.
- nutrient_topic
- Curcumin research collection; topical membership is not evidence of a direct dietary effect. · Curcumin
- organism
- Mus musculus; transfected construct species not resolved in indexed abstract
- plain_language
- The reduced metabolite did not behave like the parent compound here.
- primary_references
- [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
- tissue_or_cell_type
- JB6 epidermal cells and mouse skin
Curcumin: metabolism, signaling and nutrient connections (2026-09-17) · lines 398–409
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays · source_derived_draft · unverified_draft
### curcumin-thc-ho1-null Tetrahydrocurcumin failed to reproduce HO-1 induction in this comparison. Condition category: normal nutrient_topic: Curcumin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The reduced metabolite did not behave like the parent compound here. organism: Mus musculus; transfected construct species not resolved in indexed abstract tissue_or_cell_type: JB6 epidermal cells and mouse skin experimental_model: Mouse epidermal-cell and skin experiments, siRNA and receptor-construct assays limitations: Cell exposures and construct-origin details are not available in the indexed abstract. Results do not establish human systemic target engagement. exposure: Curcumin versus tetrahydrocurcumin; Nrf2 siRNA and Keap1 C151S construct evidence_span: {"source_cache": "artifacts/curcumin-research/31972171.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936", "start_char": 0, "end_char": 1591, "text_sha256": "0a05e877dfe677824dea390c30634719eba641ed122c2480147ce2e73bf05936"} [curcumin-p31972171] Curcumin induces stabilization of Nrf2 protein through Keap1 cysteine modification. (2020). https://pubmed.ncbi.nlm.nih.gov/31972171/ DOI: 10.1016/j.bcp.2020.113820
Complete structured claim and evidenceMyricetin increased hepatic HO-1 expression in the LPS/D-galactosamine mouse model.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse liver-injury experiment.
- limitations
- Expression is not proof of direct binding or enzyme flux; accessed in-vitro knockout details do not resolve cell species.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- A downstream defense enzyme also changed.
- primary_references
- The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 644–650
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse liver-injury experiment. · source_derived_draft · unverified_draft
## myricetin-mouse-ho1 A downstream defense enzyme also changed. Myricetin increased hepatic HO-1 expression in the LPS/D-galactosamine mouse model. Model: Mouse liver-injury experiment. Limitations: Expression is not proof of direct binding or enzyme flux; accessed in-vitro knockout details do not resolve cell species. Evidence access: Primary abstract The hepatoprotective effect of myricetin against lipopolysaccharide and D-galactosamine-induced fulminant hepatitis. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31712142/ · DOI 10.1016/j.ijbiomac.2019.11.075
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.