Component
Leukocyte adherence to vascular endothelium
Leukocyte adherence to vascular endothelium. The model and exposure of each linked claim define its scope.
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.
Where it participates (unsigned role)
Physiological-level 4PY exposure, unlike structural isomer 2PY, induced vascular VCAM-1 expression and leukocyte adherence in mice.
Experimental context and source evidence
- cross_nutrient
- Mouse vascular cell adhesion molecule 1 / Vcam1 (induced_protein); Leukocyte adherence to vascular endothelium (measured_consequence); N1-methyl-2-pyridone-5-carboxamide (2PY) (negative_comparator)
- evidence_span
- {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"}
- experimental_model
- Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures
- exposure
- Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure
- limitations
- Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Mus musculus
- plain_language
- In mice, one breakdown product directly promoted a vessel-wall adhesion response; its close chemical relative did not.
- primary_references
- [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
- tissue_or_cell_type
- Circulating metabolites and mouse vascular endothelium
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1585–1597
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures · source_derived_draft · unverified_draft
### nia-clin-4py-mouse-vcam Physiological-level 4PY exposure, unlike structural isomer 2PY, induced vascular VCAM-1 expression and leukocyte adherence in mice. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: In mice, one breakdown product directly promoted a vessel-wall adhesion response; its close chemical relative did not. organism: Mus musculus tissue_or_cell_type: Circulating metabolites and mouse vascular endothelium experimental_model: Prospective cardiac cohorts, genetic associations, and separate mouse metabolite exposures limitations: Human metabolite associations are not randomized effects of niacin intake. Renal handling and other determinants of levels matter. Mouse exposure results do not prove dietary niacin or supplements caused human events. exposure: Discovery cohort 1,162; US validation 2,331 and European validation 832; three-year cardiovascular follow-up; physiological-level mouse metabolite exposure cross_nutrient: Mouse vascular cell adhesion molecule 1 / Vcam1 (induced_protein); Leukocyte adherence to vascular endothelium (measured_consequence); N1-methyl-2-pyridone-5-carboxamide (2PY) (negative_comparator) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/ferrell2024.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19", "start_char": 0, "end_char": 2066, "text_sha256": "09530c87779c7a8db8507c847dcb29ae3b7e439967c9271dec5f7cbda6c33d19"} [nia-clin-ferrell2024] A terminal metabolite of niacin promotes vascular inflammation and contributes to cardiovascular disease risk. (2024). https://pubmed.ncbi.nlm.nih.gov/38374343/ DOI: 10.1038/s41591-023-02793-8
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.