Component

Mouse cardiac diastolic impairment

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

5 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.

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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. Dlat-transgenic mice developed the reported diastolic-impairment phenotype while systolic function was preserved during the observation period.

    Cardiomyocyte-specific mouse Dlat overexpression → Mouse cardiac diastolic impairment 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-diastolic-impairment
    evidence_location
    Figure 4M–O; Supplementary Figure S18
    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. Main-text E/A and E/e-prime directions disagree with Figure 4 and source-data columns. The data show increased ratios; the erroneous directional prose is not used as an independent finding. Transgenic age arithmetic also requires clarification.
    organism
    Mus musculus
    plain_language
    Dlat-transgenic mice developed the reported diastolic-impairment phenotype while systolic function was preserved during the observation period.
    primary_locator
    [{"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": 37, "text_sha256": "a3d0b7ba03c94c00e5cd07993ebd789dd554b51fafd62ec7937c72175c3c2a60", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM4_ESM.xlsx", "location": "figure4; E/A rows 23-32, E/e-prime rows 41-50", "sha256": "7fc506fec970a4b7e9b2f370695d82b36020de2e77a0a26112066688d52606f5"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    8 per echocardiographic group
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 388–403

    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

    Dlat-transgenic mice developed the reported diastolic-impairment phenotype while systolic function was preserved during the observation period. 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: Figure 4M–O; Supplementary Figure S18 endpoint: mouse-cardiac-diastolic-impairment 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. Main-text E/A and E/e-prime directions disagree with Figure 4 and source-data columns. The data show increased ratios; the erroneous directional prose is not used as an independent finding. Transgenic age arithmetic also requires clarification. primary_locator: [{"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": 37, "text_sha256": "a3d0b7ba03c94c00e5cd07993ebd789dd554b51fafd62ec7937c72175c3c2a60", "xml_element_id": null}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM4_ESM.xlsx", "location": "figure4; E/A rows 23-32, E/e-prime rows 41-50", "sha256": "7fc506fec970a4b7e9b2f370695d82b36020de2e77a0a26112066688d52606f5"}] plain_language: Dlat-transgenic mice developed the reported diastolic-impairment phenotype while systolic function was preserved during the observation period. sample_size: 8 per echocardiographic group
    Complete structured claim and evidence

  2. Dlat knockdown improved the reported diastolic phenotype in the two-hit HFpEF model.

    Cardiomyocyte-targeted mouse Dlat shRNA knockdown → Mouse cardiac diastolic impairment 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-diastolic-impairment
    evidence_location
    Figure 5K–M; source-data workbook figure5 L/M
    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. The prose says E/e-prime increased with improvement, whereas the plotted/source values decrease versus HFpEF control. Record the functional interpretation with this source inconsistency, not the mistaken metric direction.
    organism
    Mus musculus
    plain_language
    Dlat knockdown improved the reported diastolic phenotype 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}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM4_ESM.xlsx", "location": "figure5; E/A and E/e-prime rows 41-50", "sha256": "7fc506fec970a4b7e9b2f370695d82b36020de2e77a0a26112066688d52606f5"}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    8 per group
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 459–474

    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

    Dlat knockdown improved the reported diastolic phenotype 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: Figure 5K–M; source-data workbook figure5 L/M endpoint: mouse-cardiac-diastolic-impairment 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. The prose says E/e-prime increased with improvement, whereas the plotted/source values decrease versus HFpEF control. Record the functional interpretation with this source inconsistency, not the mistaken metric direction. 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}, {"cache": "artifacts/dlat-curation/41467_2026_70703_MOESM4_ESM.xlsx", "location": "figure5; E/A and E/e-prime rows 41-50", "sha256": "7fc506fec970a4b7e9b2f370695d82b36020de2e77a0a26112066688d52606f5"}] plain_language: Dlat knockdown improved the reported diastolic phenotype in the two-hit HFpEF model. sample_size: 8 per group
    Complete structured claim and evidence

  3. HADHA overexpression improved the reported diastolic phenotype of Dlat-transgenic mice.

    Cardiomyocyte-targeted mouse HADHA overexpression → Mouse cardiac diastolic impairment 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-diastolic-impairment
    evidence_location
    Supplementary Figure S22
    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. Mouse overexpression result; K728 was not mutated in vivo.
    organism
    Mus musculus
    plain_language
    HADHA overexpression improved the reported diastolic phenotype of Dlat-transgenic mice.
    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
    8 per group
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 495–510

    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

    HADHA overexpression improved the reported diastolic phenotype of Dlat-transgenic mice. 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 S22 endpoint: mouse-cardiac-diastolic-impairment 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. Mouse overexpression result; K728 was not mutated in vivo. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 52, "text_sha256": "74297778077d895148e1cc0c9819297c22c274b0ec6fdce0483ce8ba94ab58b4", "xml_element_id": "Par21"}] plain_language: HADHA overexpression improved the reported diastolic phenotype of Dlat-transgenic mice. sample_size: 8 per group
    Complete structured claim and evidence

  4. Nicotinamide riboside improved the reported diastolic phenotype in the mouse HFpEF model.

    Nicotinamide riboside → Mouse cardiac diastolic impairment 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-diastolic-impairment
    evidence_location
    Supplementary Figure S6
    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. Systemic metabolic effects can contribute; no human efficacy inference.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · NAD+
    organism
    Mus musculus
    plain_language
    Nicotinamide riboside improved the reported diastolic phenotype in the mouse HFpEF model.
    primary_locator
    [{"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
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 570–585

    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 the reported diastolic phenotype in the mouse 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: 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: Supplementary Figure S6 endpoint: mouse-cardiac-diastolic-impairment 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. Systemic metabolic effects can contribute; no human efficacy inference. primary_locator: [{"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 the reported diastolic phenotype in the mouse HFpEF model.
    Complete structured claim and evidence

  5. Spermidine improved the reported diastolic phenotype of mice in the HFpEF experiment.

    Spermidine → Mouse cardiac diastolic impairment source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Cardiac tissue / mitochondria
    dose
    30 mM drinking water
    duration
    10 weeks in Results
    endpoint
    mouse-cardiac-diastolic-impairment
    evidence_location
    Figure 8H–K; Supplementary Figure S24
    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. HADHA necessity for this systemic intervention was not established by a genetic blocking experiment.
    nutrient_topic
    Topical cross-reference only; no inheritance of another actor's effects. · Spermidine
    organism
    Mus musculus
    plain_language
    Spermidine improved the reported diastolic phenotype of mice in the HFpEF experiment.
    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}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    route
    Drinking water
    sample_size
    8 per group
    tissue_or_cell_type
    Cardiac tissue and cardiomyocytes

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 679–695

    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 improved the reported diastolic phenotype of mice in the HFpEF experiment. 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 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 8H–K; Supplementary Figure S24 endpoint: mouse-cardiac-diastolic-impairment exposure: spermidine limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. HADHA necessity for this systemic intervention was not established by a genetic blocking experiment. 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}] plain_language: Spermidine improved the reported diastolic phenotype of mice in the HFpEF experiment. sample_size: 8 per group
    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