Component
Cellular coenzyme Q concentration
Cellular coenzyme Q concentration. Species, exposure and limitations are retained in 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
Affected siblings with COQ5 duplications had low white-cell CoQ; the available muscle sample was also depleted.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/coq10-research/29044765.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "704d515eb76ce1074ae021346c10abee852de623057b33d287e4fad0b69d23b4", "start_char": 0, "end_char": 1271, "text_sha256": "704d515eb76ce1074ae021346c10abee852de623057b33d287e4fad0b69d23b4"}
- experimental_model
- Family sequencing and biochemical measurements
- exposure
- Biallelic COQ5 duplications; supplementation follow-up
- limitations
- Small uncontrolled genetic case series; clinical improvement cannot yield a general efficacy estimate.
- nutrient_topic
- Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
- organism
- Three human siblings
- plain_language
- A low circulating-cell pool was linked to a defined synthesis defect.
- primary_references
- [coq10-p29044765] A novel inborn error of the coenzyme Q10 biosynthesis pathway: cerebellar ataxia and static encephalomyopathy due to COQ5 C-methyltransferase deficiency. (2018). https://pubmed.ncbi.nlm.nih.gov/29044765/ DOI: 10.1002/humu.23345
- tissue_or_cell_type
- Neurologic disease and CoQ measurements
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 1035–1046
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Family sequencing and biochemical measurements · source_derived_draft · unverified_draft
### coq10-coq5-deficiency Affected siblings with COQ5 duplications had low white-cell CoQ; the available muscle sample was also depleted. Condition category: machinery_impairment nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A low circulating-cell pool was linked to a defined synthesis defect. organism: Three human siblings tissue_or_cell_type: Neurologic disease and CoQ measurements experimental_model: Family sequencing and biochemical measurements limitations: Small uncontrolled genetic case series; clinical improvement cannot yield a general efficacy estimate. exposure: Biallelic COQ5 duplications; supplementation follow-up evidence_span: {"source_cache": "artifacts/coq10-research/29044765.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "704d515eb76ce1074ae021346c10abee852de623057b33d287e4fad0b69d23b4", "start_char": 0, "end_char": 1271, "text_sha256": "704d515eb76ce1074ae021346c10abee852de623057b33d287e4fad0b69d23b4"} [coq10-p29044765] A novel inborn error of the coenzyme Q10 biosynthesis pathway: cerebellar ataxia and static encephalomyopathy due to COQ5 C-methyltransferase deficiency. (2018). https://pubmed.ncbi.nlm.nih.gov/29044765/ DOI: 10.1002/humu.23345
Complete structured claim and evidenceThe authors proposed that lower plasma CoQ could reflect loss of lipoprotein carriers rather than a statin-specific depletion mechanism.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/coq10-research/16872244.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27", "start_char": 0, "end_char": 2245, "text_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27"}
- experimental_model
- Randomized three-arm parallel study
- exposure
- Simvastatin 40 mg/day, ezetimibe 10 mg/day or both for 14 days
- limitations
- Plasma measurements and correlation; neither tissue CoQ nor mitochondrial dysfunction was demonstrated.
- nutrient_topic
- Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. · Coenzyme Q10 / CoQ10 redox system
- organism
- 72 healthy men
- plain_language
- Blood transport and intracellular deficiency are different explanations to test.
- primary_references
- [coq10-p16872244] Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16872244/ DOI: 10.2165/00002018-200629080-00007
- tissue_or_cell_type
- Plasma CoQ and lipoprotein concentrations
Coenzyme Q10: biosynthesis, electron transfer, antioxidant recycling and nutrient interactions (2026-09-17) · lines 944–955
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized three-arm parallel study · source_derived_draft · unverified_draft
### coq10-statin-carrier-interpretation The authors proposed that lower plasma CoQ could reflect loss of lipoprotein carriers rather than a statin-specific depletion mechanism. Condition category: normal nutrient_topic: Coenzyme Q10 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blood transport and intracellular deficiency are different explanations to test. organism: 72 healthy men tissue_or_cell_type: Plasma CoQ and lipoprotein concentrations experimental_model: Randomized three-arm parallel study limitations: Plasma measurements and correlation; neither tissue CoQ nor mitochondrial dysfunction was demonstrated. exposure: Simvastatin 40 mg/day, ezetimibe 10 mg/day or both for 14 days evidence_span: {"source_cache": "artifacts/coq10-research/16872244.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27", "start_char": 0, "end_char": 2245, "text_sha256": "65abd11b5f58ce1125f554d52ed5203575d7a3ba0d20b789abce16148f3b5e27"} [coq10-p16872244] Effect of ezetimibe and/or simvastatin on coenzyme Q10 levels in plasma: a randomised trial. (2006). https://pubmed.ncbi.nlm.nih.gov/16872244/ DOI: 10.2165/00002018-200629080-00007
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.