Component
Proinflammatory SASP in human IMR90 fibroblasts
Context-specific entity; species, compartment and exposure are stated on each 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
NAMPT-supported NAD metabolism sustained glycolysis and respiration and promoted a proinflammatory SASP through the AMPK–p53–p38/NF-kappaB regulatory network in the tested senescent cells.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown.
- limitations
- Not proof that NAD supplementation causes cancer in humans or that all senescent cells respond alike.
- nutrient_topic
- NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
- plain_language
- Supporting cellular metabolism can also support inflammatory secretion.
- primary_references
- NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 156–162
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown. · source_derived_draft · unverified_draft
## nad-plus-nampt-sasp Supporting cellular metabolism can also support inflammatory secretion. NAMPT-supported NAD metabolism sustained glycolysis and respiration and promoted a proinflammatory SASP through the AMPK–p53–p38/NF-kappaB regulatory network in the tested senescent cells. Model: Human IMR90 fibroblast senescence; NAMPT inhibition and knockdown. Limitations: Not proof that NAD supplementation causes cancer in humans or that all senescent cells respond alike. Evidence access: Primary full text NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
Complete structured claim and evidence
Where it participates (unsigned role)
HMGA1-dependent NAMPT expression contributed to increased NAD metabolism and the proinflammatory secretory phenotype in oncogene-induced senescent human IMR90 fibroblasts.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Human fibroblast oncogene-induced senescence with genetic perturbations.
- limitations
- Senescence type matters; replicative and mitochondrial-dysfunction senescence need not share this pattern.
- nutrient_topic
- NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
- plain_language
- A gene regulator can increase NAD salvage in a cell that is already senescent.
- primary_references
- NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 148–154
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human fibroblast oncogene-induced senescence with genetic perturbations. · source_derived_draft · unverified_draft
## nad-plus-hmga-nampt A gene regulator can increase NAD salvage in a cell that is already senescent. HMGA1-dependent NAMPT expression contributed to increased NAD metabolism and the proinflammatory secretory phenotype in oncogene-induced senescent human IMR90 fibroblasts. Model: Human fibroblast oncogene-induced senescence with genetic perturbations. Limitations: Senescence type matters; replicative and mitochondrial-dysfunction senescence need not share this pattern. Evidence access: Primary full text NAD+ metabolism governs the proinflammatory senescence-associated secretome. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30778219/ · DOI 10.1038/s41556-019-0287-4
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.