Senescent cells promote tissue NAD + decline during ageing via the activation of CD38 + macrophages.
Level 5 - mechanism / opinion, no new human data
Preclinical laboratory mechanistic research without clinical data
PubMed 33199924 · doi:10.1038/s42255-020-00305-3
What was done
Investigated the mechanisms connecting cellular senescence, macrophage accumulation, and tissue NAD+ decline during aging and acute inflammation, specifically examining CD38 expression and NADase activity across macrophage subtypes in metabolic tissues including visceral white adipose tissue and liver.
What was found
The abstract reports no numerical values, sample sizes, or effect estimates. It reports that pro-inflammatory M1-like macrophages (unlike naive or M2 macrophages) accumulate in visceral white adipose tissue and liver during aging and inflammation, exhibit elevated CD38 expression and CD38-dependent NADase activity, and drive tissue NAD decline. Additionally, senescent cell secretions (SASP) were found to induce macrophage proliferation and CD38 expression.
Why it matters
Identifies a mechanistic pathway linking senescent cell accumulation to macrophage-driven CD38 NADase activity and subsequent tissue NAD+ depletion during aging.
Limits
The abstract contains no quantitative data, sample sizes, or species details. Findings are purely preclinical and bench-based without direct human clinical trial verification.
Cited by
- supports Chronic immune activation results in a deficiency of intracellular NAD within immune cells.