Component
Mouse CD38
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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 it acts on
The study linked extracellular CD38 enzymatic activity to NMN degradation and lower precursor availability; selective blockade of ecto-CD38 increased NAD+ in mouse experiments.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Mouse biochemical, cellular and ecto-CD38 antibody experiments.
- limitations
- Not established clinical benefit from an over-the-counter CD38 inhibitor.
- nutrient_topic
- NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
- plain_language
- A precursor can be destroyed before a neighboring cell uses it.
- primary_references
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 116–122
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse biochemical, cellular and ecto-CD38 antibody experiments. · source_derived_draft · unverified_draft
## nad-plus-ecto-cd38-nmn A precursor can be destroyed before a neighboring cell uses it. The study linked extracellular CD38 enzymatic activity to NMN degradation and lower precursor availability; selective blockade of ecto-CD38 increased NAD+ in mouse experiments. Model: Mouse biochemical, cellular and ecto-CD38 antibody experiments. Limitations: Not established clinical benefit from an over-the-counter CD38 inhibitor. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
Complete structured claim and evidence
What acts on it
Aged mouse liver and white adipose tissue accumulated CD38-positive immune cells, including macrophages/monocytes, with increased expression per cell in several comparisons.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Young versus aged mice; flow cytometry, histology and macrophage experiments.
- limitations
- Cell abundance and expression observations do not alone quantify absolute tissue NAD flux.
- nutrient_topic
- NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
- plain_language
- More NAD-consuming immune cells can change a tissue metabolite pool.
- primary_references
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 100–106
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Young versus aged mice; flow cytometry, histology and macrophage experiments. · source_derived_draft · unverified_draft
## nad-plus-aging-cd38 More NAD-consuming immune cells can change a tissue metabolite pool. Aged mouse liver and white adipose tissue accumulated CD38-positive immune cells, including macrophages/monocytes, with increased expression per cell in several comparisons. Model: Young versus aged mice; flow cytometry, histology and macrophage experiments. Limitations: Cell abundance and expression observations do not alone quantify absolute tissue NAD flux. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
Complete structured claim and evidenceSenescent-cell-associated inflammatory signals promoted CD38 expression; reducing senescent-cell burden partially restored NAD+ in the reported mouse experiments.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Senescent-cell conditioned media and mouse interventions.
- limitations
- Partial rescue supports a contributing mechanism, not a single cause of every age-associated NAD decline.
- nutrient_topic
- NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
- plain_language
- Signals from one cell population can change NAD availability in another.
- primary_references
- CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 108–114
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Senescent-cell conditioned media and mouse interventions. · source_derived_draft · unverified_draft
## nad-plus-sasp-cd38 Signals from one cell population can change NAD availability in another. Senescent-cell-associated inflammatory signals promoted CD38 expression; reducing senescent-cell burden partially restored NAD+ in the reported mouse experiments. Model: Senescent-cell conditioned media and mouse interventions. Limitations: Partial rescue supports a contributing mechanism, not a single cause of every age-associated NAD decline. Evidence access: Primary full text CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD+ and NMN levels. · 2020 · https://pubmed.ncbi.nlm.nih.gov/33199925/ · DOI 10.1038/s42255-020-00298-z
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.