Component

Total iron in isolated human-cell mitochondria

3 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. K68R HMOX2 re-expression failed to restore mitochondrial iron as wild-type HMOX2 did in HMOX2-knockout HeLa cells.

    K68R HMOX2 re-expression in HMOX2-null HeLa cells → Total iron in isolated human-cell mitochondria source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    Stable re-expression in HMOX2 KO clone 1; ICP-MS total iron; comparison with wild-type re-expression
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Figure 4f
    primary_references
    https://doi.org/10.1038/s41556-026-01974-0

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 72–80

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    K68R HMOX2 re-expression failed to restore mitochondrial iron as wild-type HMOX2 did in HMOX2-knockout HeLa cells. primary_references: https://doi.org/10.1038/s41556-026-01974-0 primary_locator: Figure 4f evidence_cache: artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: Stable re-expression in HMOX2 KO clone 1; ICP-MS total iron; comparison with wild-type re-expression limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence

  2. HMOX2 knockout reduced total iron measured in isolated HeLa mitochondria.

    HMOX2 knockout in HeLa cells → Total iron in isolated human-cell mitochondria source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    Stable CRISPR knockout; ICP-MS after digestion; pg iron per microgram mitochondrial protein; three independent experiments
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Figure 4c
    primary_references
    https://doi.org/10.1038/s41556-026-01974-0

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 61–69

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    HMOX2 knockout reduced total iron measured in isolated HeLa mitochondria. primary_references: https://doi.org/10.1038/s41556-026-01974-0 primary_locator: Figure 4c evidence_cache: artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: Stable CRISPR knockout; ICP-MS after digestion; pg iron per microgram mitochondrial protein; three independent experiments limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    Complete structured claim and evidence

  3. VAPB knockout reduced total iron measured in isolated HeLa mitochondria.

    VAPB knockout in HeLa cells → Total iron in isolated human-cell mitochondria source_derived_draftungraded
    Experimental context and source evidence
    access_level
    selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review
    evidence_cache
    artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a
    experimental_model
    HeLa; MERBiT reporter derivative where stated
    exposure
    Stable CRISPR knockout; ICP-MS after digestion; pg metal per microgram mitochondrial protein; three independent experiments
    limitations
    Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    organism
    Human
    primary_locator
    Figure 4g
    primary_references
    https://doi.org/10.1038/s41556-026-01974-0

    Glutathione, ER-mitochondria contacts, and iron: observed components · lines 83–91

    Targeted primary-literature curation, 2026-09-20. DOIs 10.1038/s41467-025-56666-4 and 10.1038/s41556-026-01974-0. · supports · Human HeLa cells · source_derived_draft · unverified_draft

    VAPB knockout reduced total iron measured in isolated HeLa mitochondria. primary_references: https://doi.org/10.1038/s41556-026-01974-0 primary_locator: Figure 4g evidence_cache: artifacts/discovery-research/round4-sources/s41556-026-01974-0-web.json; SHA256 6971539ed35950faaf1931771badfd7fbad98541e4ffcb56177e63be586de40a access_level: selected_primary_main_text_and_legends; cached web/indexed passages, not complete supplement review organism: Human experimental_model: HeLa; MERBiT reporter derivative where stated exposure: Stable CRISPR knockout; ICP-MS after digestion; pg metal per microgram mitochondrial protein; three independent experiments limitations: Selected primary main-text Results and figure legends reviewed; supplementary images not independently inspected. These two papers share authors and are not independent replication. They do not test whether SLC25A39-loss-induced contacts increase HMOX2-dependent iron delivery. ICP-MS measures total iron, not labile iron or transport flux. Contact loss affecting an outcome does not establish that increasing contacts increases it. Ubiquitination/activity readouts do not establish direct enzymatic activation or the outer-membrane iron transport machinery. No clinical or pulmonary-endothelial effect is inferred.
    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