Component
Mouse cardiac mitochondrial protein lysine acetylation
Study-specific entity. Experimental conditions and evidence limits remain on each linked claim.
1 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 acts on it
Cardiac Dlat knockdown reduced mitochondrial protein hyperacetylation in the two-hit HFpEF model.
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-mitochondrial-protein-acetylation
- evidence_location
- Figure 5C/D
- 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.
- organism
- Mus musculus
- plain_language
- Cardiac Dlat knockdown reduced mitochondrial protein hyperacetylation 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
- 6 overall; 3 per individual protein panel
- tissue_or_cell_type
- Cardiac tissue and cardiomyocytes
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 424–439
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 reduced mitochondrial protein hyperacetylation 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 5C/D endpoint: mouse-mitochondrial-protein-acetylation 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. 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 reduced mitochondrial protein hyperacetylation in the two-hit HFpEF model. sample_size: 6 overall; 3 per individual protein panel
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.