Component

Rat cardiac fatty-acid oxidation capacity

Study-specific entity. Experimental conditions and evidence limits remain on each linked claim.

4 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. 3-TYP reduced fatty-acid-supported respiration in neonatal rat cardiomyocytes.

    3-TYP experimental SIRT3 inhibitor → Rat cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Mitochondria or cell lysate, depending on assay
    dose
    Compound concentration not established in reviewed text
    duration
    Treatment endpoint timing not established in reviewed text
    endpoint
    rat-cardiac-fao
    evidence_location
    Figure 2B–E
    experimental_model
    Pharmacological 3-TYP experiment; NR co-treatment where stated
    exposure
    3-typ
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported SIRT3-inhibitor experiment; do not assume complete target specificity.
    organism
    Rattus norvegicus host cells; construct species may be unspecified
    plain_language
    3-TYP reduced fatty-acid-supported respiration in neonatal rat cardiomyocytes.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 23, "text_sha256": "08f11746524e975c9e1a5e3d53de363a6762891bc05afffbd711f347867ac842", "xml_element_id": "Par10"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Neonatal rat ventricular cardiomyocytes (NRVCMs)

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 605–620

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Pharmacological 3-TYP experiment; NR co-treatment where stated · source_derived_draft · unverified_draft

    3-TYP reduced fatty-acid-supported respiration in neonatal rat cardiomyocytes. organism: Rattus norvegicus host cells; construct species may be unspecified tissue_or_cell_type: Neonatal rat ventricular cardiomyocytes (NRVCMs) experimental_model: Pharmacological 3-TYP experiment; NR co-treatment where stated compartment: Mitochondria or cell lysate, depending on assay dose: Compound concentration not established in reviewed text duration: Treatment endpoint timing not established in reviewed text primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 2B–E endpoint: rat-cardiac-fao exposure: 3-typ limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported SIRT3-inhibitor experiment; do not assume complete target specificity. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 23, "text_sha256": "08f11746524e975c9e1a5e3d53de363a6762891bc05afffbd711f347867ac842", "xml_element_id": "Par10"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}] plain_language: 3-TYP reduced fatty-acid-supported respiration in neonatal rat cardiomyocytes. sample_size: 4 biological replicates
    Complete structured claim and evidence

  2. NR co-treatment opposed the impaired FAO-associated respiration in the 3-TYP rat-cell experiment.

    Nicotinamide riboside → Rat cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Mitochondria or cell lysate, depending on assay
    dose
    Compound concentration not established in reviewed text
    duration
    Treatment endpoint timing not established in reviewed text
    endpoint
    rat-cardiac-fao
    evidence_location
    Figure 2A–G
    experimental_model
    Pharmacological 3-TYP experiment; NR co-treatment where stated
    exposure
    nicotinamide-riboside
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. The figure tests 3-TYP plus NR; do not mislabel it as an NR-alone dose-response experiment.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · NAD+
    organism
    Rattus norvegicus host cells; construct species may be unspecified
    plain_language
    NR co-treatment opposed the impaired FAO-associated respiration in the 3-TYP rat-cell experiment.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 23, "text_sha256": "08f11746524e975c9e1a5e3d53de363a6762891bc05afffbd711f347867ac842", "xml_element_id": "Par10"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 respiratory replicates; 6 staining replicates
    tissue_or_cell_type
    Neonatal rat ventricular cardiomyocytes (NRVCMs)

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 623–638

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Pharmacological 3-TYP experiment; NR co-treatment where stated · source_derived_draft · unverified_draft

    NR co-treatment opposed the impaired FAO-associated respiration in the 3-TYP rat-cell experiment. organism: Rattus norvegicus host cells; construct species may be unspecified tissue_or_cell_type: Neonatal rat ventricular cardiomyocytes (NRVCMs) experimental_model: Pharmacological 3-TYP experiment; NR co-treatment where stated compartment: Mitochondria or cell lysate, depending on assay dose: Compound concentration not established in reviewed text duration: Treatment endpoint timing not established in reviewed text primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 2A–G endpoint: rat-cardiac-fao exposure: nicotinamide-riboside limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. The figure tests 3-TYP plus NR; do not mislabel it as an NR-alone dose-response experiment. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 23, "text_sha256": "08f11746524e975c9e1a5e3d53de363a6762891bc05afffbd711f347867ac842", "xml_element_id": "Par10"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}] plain_language: NR co-treatment opposed the impaired FAO-associated respiration in the 3-TYP rat-cell experiment. sample_size: 4 respiratory replicates; 6 staining replicates
    Complete structured claim and evidence

  3. Dlat overexpression lowered palmitate-supported oxygen consumption in neonatal rat cardiomyocytes.

    Dlat overexpression in neonatal rat ventricular cardiomyocytes → Rat cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Mitochondria or cell lysate, depending on assay
    dose
    Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods
    duration
    Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified
    endpoint
    rat-cardiac-fao
    evidence_location
    Seahorse palmitate oxidation stress test; Figure 3L–N
    experimental_model
    Adenoviral/cell perturbation study
    exposure
    rat-dlat-overexpression
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. OCR is a respiratory readout rather than a complete FAO flux balance. Etomoxir concentration was not specified in the reviewed methods.
    organism
    Rattus norvegicus host cells; construct species may be unspecified
    plain_language
    Dlat overexpression lowered palmitate-supported oxygen consumption in neonatal rat cardiomyocytes.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 31, "text_sha256": "74c923c72ae212e33ea648b25e8bc69db773a547139d5fa5b15971076fdeddd0", "xml_element_id": "Par13"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 30, "text_sha256": "c2e9b88e22dc6b77f227fe9d4192d471b12452fe1e59280543fcc219fed2414f", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 90, "text_sha256": "9acf1ca568eece887ec72ad83ba8e593471afa5810e005762d0d3cbcfd80e700", "xml_element_id": "Par40"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Neonatal rat ventricular cardiomyocytes (NRVCMs)

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 196–211

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Adenoviral/cell perturbation study · source_derived_draft · unverified_draft

    Dlat overexpression lowered palmitate-supported oxygen consumption in neonatal rat cardiomyocytes. organism: Rattus norvegicus host cells; construct species may be unspecified tissue_or_cell_type: Neonatal rat ventricular cardiomyocytes (NRVCMs) experimental_model: Adenoviral/cell perturbation study compartment: Mitochondria or cell lysate, depending on assay dose: Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods duration: Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Seahorse palmitate oxidation stress test; Figure 3L–N endpoint: rat-cardiac-fao exposure: rat-dlat-overexpression limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. OCR is a respiratory readout rather than a complete FAO flux balance. Etomoxir concentration was not specified in the reviewed methods. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 31, "text_sha256": "74c923c72ae212e33ea648b25e8bc69db773a547139d5fa5b15971076fdeddd0", "xml_element_id": "Par13"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 30, "text_sha256": "c2e9b88e22dc6b77f227fe9d4192d471b12452fe1e59280543fcc219fed2414f", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 90, "text_sha256": "9acf1ca568eece887ec72ad83ba8e593471afa5810e005762d0d3cbcfd80e700", "xml_element_id": "Par40"}] plain_language: Dlat overexpression lowered palmitate-supported oxygen consumption in neonatal rat cardiomyocytes. sample_size: 4 biological replicates
    Complete structured claim and evidence

  4. WY14643 treatment restored fatty-acid-supported respiration in Dlat-overexpressing rat cardiomyocytes.

    WY14643 experimental PPAR-alpha agonist → Rat cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Mitochondria or cell lysate, depending on assay
    dose
    Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods
    duration
    Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified
    endpoint
    rat-cardiac-fao
    evidence_location
    Supplementary Figure S9
    experimental_model
    Adenoviral/cell perturbation study
    exposure
    wy14643
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. PPAR-alpha agonist experiment; dose and duration not specified in the reviewed text. It does not establish selective action on HADHA.
    organism
    Rattus norvegicus host cells; construct species may be unspecified
    plain_language
    WY14643 treatment restored fatty-acid-supported respiration in Dlat-overexpressing rat cardiomyocytes.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 32, "text_sha256": "ea1ec18a5210aa68822ce1416ae850de5ce871e100938a13a2c1dcc49c444731", "xml_element_id": "Par14"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    tissue_or_cell_type
    Neonatal rat ventricular cardiomyocytes (NRVCMs)

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 318–332

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Adenoviral/cell perturbation study · source_derived_draft · unverified_draft

    WY14643 treatment restored fatty-acid-supported respiration in Dlat-overexpressing rat cardiomyocytes. organism: Rattus norvegicus host cells; construct species may be unspecified tissue_or_cell_type: Neonatal rat ventricular cardiomyocytes (NRVCMs) experimental_model: Adenoviral/cell perturbation study compartment: Mitochondria or cell lysate, depending on assay dose: Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods duration: Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Supplementary Figure S9 endpoint: rat-cardiac-fao exposure: wy14643 limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. PPAR-alpha agonist experiment; dose and duration not specified in the reviewed text. It does not establish selective action on HADHA. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 32, "text_sha256": "ea1ec18a5210aa68822ce1416ae850de5ce871e100938a13a2c1dcc49c444731", "xml_element_id": "Par14"}] plain_language: WY14643 treatment restored fatty-acid-supported respiration in Dlat-overexpressing rat cardiomyocytes.
    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