Component

Mouse cardiac fatty-acid oxidation capacity

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

6 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. Cardiac-specific Dlat overexpression reduced octanoylcarnitine-supported respiration in mouse heart preparations.

    Cardiomyocyte-specific mouse Dlat overexpression → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    Tamoxifen-induced genetic overexpression; vector/induction dose not established in this extraction
    duration
    Transgenic induction age and observation interval differ across passages; exact interval unresolved
    endpoint
    mouse-cardiac-fao
    evidence_location
    Oroboros respirometry; Figure 4I–K
    experimental_model
    Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated
    exposure
    mouse-dlat-overexpression
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Substrate-supported respiratory capacity, not an intact-animal FAO flux. Methods call the substrate both octanoylcarnitine and palmitoyl-carnitine; retain the explicit reagent as reported, with ambiguity flagged.
    organism
    Mus musculus
    plain_language
    Cardiac-specific Dlat overexpression reduced octanoylcarnitine-supported respiration in mouse heart preparations.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 35, "text_sha256": "28124428b0c4afe43ebd39f6ba3ab50da327de54267a02a3bdd81c53aa5c6743", "xml_element_id": "Par16"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 37, "text_sha256": "a3d0b7ba03c94c00e5cd07993ebd789dd554b51fafd62ec7937c72175c3c2a60", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 38, "text_sha256": "e2abb7e90e9e5c62be80dfa1edc1640c63d0d2e3e053cc6c5fb631e57372200a", "xml_element_id": "Par17"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 88, "text_sha256": "da214c15c67429e79f372bef6347c2c7bc604429178f3a9db5651425732f37b4", "xml_element_id": "Par39"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 353–368

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated · source_derived_draft · unverified_draft

    Cardiac-specific Dlat overexpression reduced octanoylcarnitine-supported respiration in mouse heart preparations. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated compartment: Cardiac tissue / mitochondria dose: Tamoxifen-induced genetic overexpression; vector/induction dose not established in this extraction duration: Transgenic induction age and observation interval differ across passages; exact interval unresolved primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Oroboros respirometry; Figure 4I–K endpoint: mouse-cardiac-fao exposure: mouse-dlat-overexpression limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Substrate-supported respiratory capacity, not an intact-animal FAO flux. Methods call the substrate both octanoylcarnitine and palmitoyl-carnitine; retain the explicit reagent as reported, with ambiguity flagged. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 35, "text_sha256": "28124428b0c4afe43ebd39f6ba3ab50da327de54267a02a3bdd81c53aa5c6743", "xml_element_id": "Par16"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 37, "text_sha256": "a3d0b7ba03c94c00e5cd07993ebd789dd554b51fafd62ec7937c72175c3c2a60", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 38, "text_sha256": "e2abb7e90e9e5c62be80dfa1edc1640c63d0d2e3e053cc6c5fb631e57372200a", "xml_element_id": "Par17"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 88, "text_sha256": "da214c15c67429e79f372bef6347c2c7bc604429178f3a9db5651425732f37b4", "xml_element_id": "Par39"}] plain_language: Cardiac-specific Dlat overexpression reduced octanoylcarnitine-supported respiration in mouse heart preparations. sample_size: 4 biological replicates
    Complete structured claim and evidence

  2. Partial Dlat knockdown did not substantially change the reported FAO capacity of control mouse hearts.

    Cardiomyocyte-targeted mouse Dlat shRNA knockdown → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    Partial AAV9-mediated Dlat knockdown; vector dose unresolved
    duration
    Endpoint interval not resolved for this control arm
    endpoint
    mouse-cardiac-fao
    evidence_location
    Control+AAV9-sh-Dlat versus control+AAV9-NC; Figure 5
    experimental_model
    Non-HFpEF control hearts with partial AAV9-mediated Dlat knockdown
    exposure
    mouse-dlat-knockdown
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. A context-specific null finding with partial knockdown; not proof that total Dlat loss is harmless.
    organism
    Mus musculus
    plain_language
    Partial Dlat knockdown did not substantially change the reported FAO capacity of control mouse hearts.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 40, "text_sha256": "243609ee6c00a8f0af6ff98eb44fa8397862deb054738dfa97ffabdbb7be4763", "xml_element_id": "Par18"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 42, "text_sha256": "6736653063633e10bc6238c895766205418e072440d0bb94d0415def1a9ec579", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 442–456

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Non-HFpEF control hearts with partial AAV9-mediated Dlat knockdown · source_derived_draft · unverified_draft

    Partial Dlat knockdown did not substantially change the reported FAO capacity of control mouse hearts. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Non-HFpEF control hearts with partial AAV9-mediated Dlat knockdown compartment: Cardiac tissue / mitochondria dose: Partial AAV9-mediated Dlat knockdown; vector dose unresolved duration: Endpoint interval not resolved for this control arm primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Control+AAV9-sh-Dlat versus control+AAV9-NC; Figure 5 endpoint: mouse-cardiac-fao exposure: mouse-dlat-knockdown limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. A context-specific null finding with partial knockdown; not proof that total Dlat loss is harmless. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 40, "text_sha256": "243609ee6c00a8f0af6ff98eb44fa8397862deb054738dfa97ffabdbb7be4763", "xml_element_id": "Par18"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 42, "text_sha256": "6736653063633e10bc6238c895766205418e072440d0bb94d0415def1a9ec579", "xml_element_id": null}] plain_language: Partial Dlat knockdown did not substantially change the reported FAO capacity of control mouse hearts.
    Complete structured claim and evidence

  3. Cardiac Dlat knockdown improved substrate-supported respiration in the two-hit HFpEF model.

    Cardiomyocyte-targeted mouse Dlat shRNA knockdown → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    Two-hit model: 60% fat-calorie diet and L-NAME 0.5 g/L drinking water; vector dose not reported in reviewed text
    duration
    Two-hit protocol 15 weeks. Transgenic age/induction wording differs across passages; do not infer one exact interval
    endpoint
    mouse-cardiac-fao
    evidence_location
    AAV9-cTnT-Dlat shRNA and Oroboros respirometry; Figure 5E–G
    experimental_model
    Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated
    exposure
    mouse-dlat-knockdown
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Partial knockdown, not complete deletion; not evidence that systemic DLAT inhibition is safe.
    organism
    Mus musculus
    plain_language
    Cardiac Dlat knockdown improved substrate-supported respiration in the two-hit HFpEF model.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 40, "text_sha256": "243609ee6c00a8f0af6ff98eb44fa8397862deb054738dfa97ffabdbb7be4763", "xml_element_id": "Par18"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 42, "text_sha256": "6736653063633e10bc6238c895766205418e072440d0bb94d0415def1a9ec579", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 406–421

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated · source_derived_draft · unverified_draft

    Cardiac Dlat knockdown improved substrate-supported respiration in the two-hit HFpEF model. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated compartment: Cardiac tissue / mitochondria dose: Two-hit model: 60% fat-calorie diet and L-NAME 0.5 g/L drinking water; vector dose not reported in reviewed text duration: Two-hit protocol 15 weeks. Transgenic age/induction wording differs across passages; do not infer one exact interval primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: AAV9-cTnT-Dlat shRNA and Oroboros respirometry; Figure 5E–G endpoint: mouse-cardiac-fao exposure: mouse-dlat-knockdown limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Partial knockdown, not complete deletion; not evidence that systemic DLAT inhibition is safe. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 40, "text_sha256": "243609ee6c00a8f0af6ff98eb44fa8397862deb054738dfa97ffabdbb7be4763", "xml_element_id": "Par18"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 42, "text_sha256": "6736653063633e10bc6238c895766205418e072440d0bb94d0415def1a9ec579", "xml_element_id": null}] plain_language: Cardiac Dlat knockdown improved substrate-supported respiration in the two-hit HFpEF model. sample_size: 4 biological replicates
    Complete structured claim and evidence

  4. AAV9-mediated HADHA overexpression restored FAO-associated respiration in Dlat-transgenic mouse hearts.

    Cardiomyocyte-targeted mouse HADHA overexpression → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    Tamoxifen-induced genetic overexpression; vector/induction dose not established in this extraction
    duration
    Transgenic induction age and observation interval differ across passages; exact interval unresolved
    endpoint
    mouse-cardiac-fao
    evidence_location
    Supplementary Figure S21
    experimental_model
    Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated
    exposure
    mouse-hadha-overexpression
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Wild-type HADHA overexpression, not a K728R mouse rescue; increased enzyme abundance does not isolate the acetylation-site mechanism.
    organism
    Mus musculus
    plain_language
    AAV9-mediated HADHA overexpression restored FAO-associated respiration in Dlat-transgenic mouse hearts.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 52, "text_sha256": "74297778077d895148e1cc0c9819297c22c274b0ec6fdce0483ce8ba94ab58b4", "xml_element_id": "Par21"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 477–492

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated · source_derived_draft · unverified_draft

    AAV9-mediated HADHA overexpression restored FAO-associated respiration in Dlat-transgenic mouse hearts. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Conditional cardiac Dlat-transgenic mice; HADHA AAV9 rescue where stated compartment: Cardiac tissue / mitochondria dose: Tamoxifen-induced genetic overexpression; vector/induction dose not established in this extraction duration: Transgenic induction age and observation interval differ across passages; exact interval unresolved primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Supplementary Figure S21 endpoint: mouse-cardiac-fao exposure: mouse-hadha-overexpression limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Wild-type HADHA overexpression, not a K728R mouse rescue; increased enzyme abundance does not isolate the acetylation-site mechanism. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 52, "text_sha256": "74297778077d895148e1cc0c9819297c22c274b0ec6fdce0483ce8ba94ab58b4", "xml_element_id": "Par21"}] plain_language: AAV9-mediated HADHA overexpression restored FAO-associated respiration in Dlat-transgenic mouse hearts. sample_size: 4 biological replicates
    Complete structured claim and evidence

  5. Nicotinamide riboside improved substrate-supported respiration in HFpEF mouse hearts.

    Nicotinamide riboside → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    400 mg/kg/day
    duration
    Figure 2 treatment timeline; exact intervention duration not independently resolved from narrative
    endpoint
    mouse-cardiac-fao
    evidence_location
    Figure 2M–O
    experimental_model
    Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as 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. Mouse pharmacological exposure, not a human supplement efficacy or dose claim.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · NAD+
    organism
    Mus musculus
    plain_language
    Nicotinamide riboside improved substrate-supported respiration in HFpEF mouse hearts.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 26, "text_sha256": "61dd26202087c725d9dc65345339778ed43192b3f765d05fa8a311a6e1944b34", "xml_element_id": "Par11"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 72, "text_sha256": "2b1ada63fe6c48d4296bbfb14a97940ac4a866b1d5171b0923851ec72f88ab15", "xml_element_id": "Par31"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    route
    Oral gavage
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 551–567

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated · source_derived_draft · unverified_draft

    Nicotinamide riboside improved substrate-supported respiration in HFpEF mouse hearts. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated compartment: Cardiac tissue / mitochondria dose: 400 mg/kg/day duration: Figure 2 treatment timeline; exact intervention duration not independently resolved from narrative route: Oral gavage primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 2M–O endpoint: mouse-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. Mouse pharmacological exposure, not a human supplement efficacy or dose claim. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 25, "text_sha256": "1814242d6194ed4e0b3ab78287e20f85b6bc243051183d0f24d9034c3a930257", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 26, "text_sha256": "61dd26202087c725d9dc65345339778ed43192b3f765d05fa8a311a6e1944b34", "xml_element_id": "Par11"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 72, "text_sha256": "2b1ada63fe6c48d4296bbfb14a97940ac4a866b1d5171b0923851ec72f88ab15", "xml_element_id": "Par31"}] plain_language: Nicotinamide riboside improved substrate-supported respiration in HFpEF mouse hearts. sample_size: 4 biological replicates
    Complete structured claim and evidence

  6. Spermidine-treated HFpEF mice showed improved fatty-acid-supported cardiac respiration.

    Spermidine → Mouse cardiac fatty-acid oxidation capacity source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    30 mM drinking water, as reported
    duration
    10 weeks in Results
    endpoint
    mouse-cardiac-fao
    evidence_location
    Figure 8C–E
    experimental_model
    Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated
    exposure
    spermidine
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Mouse model; no human dose or efficacy inference. Treatment duration differs from the general 15-week model description.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · Spermidine
    organism
    Mus musculus
    plain_language
    Spermidine-treated HFpEF mice showed improved fatty-acid-supported cardiac respiration.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 54, "text_sha256": "ecfe210aa0338ec52935a354f2bcc46289d65981b7b09fd4299e4e4f2fac4254", "xml_element_id": "Par22"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 56, "text_sha256": "b4baf8321f41630eff2d66a4181f2907f674041d430ba7878fd278f33d4141cf", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 72, "text_sha256": "2b1ada63fe6c48d4296bbfb14a97940ac4a866b1d5171b0923851ec72f88ab15", "xml_element_id": "Par31"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    route
    Drinking water
    sample_size
    4 biological replicates
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 660–676

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated · source_derived_draft · unverified_draft

    Spermidine-treated HFpEF mice showed improved fatty-acid-supported cardiac respiration. organism: Mus musculus tissue_or_cell_type: Cardiac tissue and cardiomyocytes experimental_model: Mouse two-hit HFpEF model: 60% fat-calorie diet plus L-NAME 0.5 g/L drinking water; additional intervention as stated compartment: Cardiac tissue / mitochondria dose: 30 mM drinking water, as reported duration: 10 weeks in Results route: Drinking water primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: Figure 8C–E endpoint: mouse-cardiac-fao exposure: spermidine limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Mouse model; no human dose or efficacy inference. Treatment duration differs from the general 15-week model description. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 54, "text_sha256": "ecfe210aa0338ec52935a354f2bcc46289d65981b7b09fd4299e4e4f2fac4254", "xml_element_id": "Par22"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 56, "text_sha256": "b4baf8321f41630eff2d66a4181f2907f674041d430ba7878fd278f33d4141cf", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 72, "text_sha256": "2b1ada63fe6c48d4296bbfb14a97940ac4a866b1d5171b0923851ec72f88ab15", "xml_element_id": "Par31"}] plain_language: Spermidine-treated HFpEF mice showed improved fatty-acid-supported cardiac respiration. sample_size: 4 biological replicates
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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