Component
Cardiomyocyte-targeted mouse HADHA overexpression
Study-specific entity. Experimental conditions and evidence limits remain on each linked claim.
2 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
HADHA overexpression improved the reported diastolic phenotype of Dlat-transgenic mice.
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 evidenceAAV9-mediated HADHA overexpression restored FAO-associated respiration in Dlat-transgenic mouse hearts.
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
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.