Component
Rat cardiac mitochondrial protein lysine acetylation
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 acts on it
3-TYP treatment increased mitochondrial protein acetylation in neonatal rat cardiomyocytes.
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-mitochondrial-protein-acetylation
- evidence_location
- Figure 2A
- 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. Pharmacological inhibition is not a Sirt3 genetic-specificity experiment; concentration not specified in reviewed text.
- organism
- Rattus norvegicus host cells; construct species may be unspecified
- plain_language
- 3-TYP treatment increased mitochondrial protein acetylation 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
- tissue_or_cell_type
- Neonatal rat ventricular cardiomyocytes (NRVCMs)
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 588–602
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 treatment increased mitochondrial protein acetylation 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 2A endpoint: rat-mitochondrial-protein-acetylation 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. Pharmacological inhibition is not a Sirt3 genetic-specificity experiment; concentration not specified in reviewed text. 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 treatment increased mitochondrial protein acetylation in neonatal rat cardiomyocytes.
Complete structured claim and evidenceDlat overexpression increased mitochondrial protein acetylation in neonatal rat cardiomyocytes.
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-mitochondrial-protein-acetylation
- evidence_location
- Mitochondrial immunoblot; Figure 3G/H
- 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. Other FAO proteins showed increased acetylation, but direct catalytic modification of each was not established.
- organism
- Rattus norvegicus host cells; construct species may be unspecified
- plain_language
- Dlat overexpression increased mitochondrial protein acetylation in neonatal rat cardiomyocytes.
- primary_locator
- [{"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": 31, "text_sha256": "74c923c72ae212e33ea648b25e8bc69db773a547139d5fa5b15971076fdeddd0", "xml_element_id": "Par13"}]
- primary_references
- https://doi.org/10.1038/s41467-026-70703-w
- sample_size
- 6 overall; 3 per individual protein panel
- tissue_or_cell_type
- Neonatal rat ventricular cardiomyocytes (NRVCMs)
DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 232–247
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 increased mitochondrial protein acetylation 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: Mitochondrial immunoblot; Figure 3G/H endpoint: rat-mitochondrial-protein-acetylation 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. Other FAO proteins showed increased acetylation, but direct catalytic modification of each was not established. primary_locator: [{"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": 31, "text_sha256": "74c923c72ae212e33ea648b25e8bc69db773a547139d5fa5b15971076fdeddd0", "xml_element_id": "Par13"}] plain_language: Dlat overexpression increased mitochondrial protein acetylation in neonatal rat cardiomyocytes. 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.