Study summary · research use only
CD38 ecto-enzyme in immune cells is induced during aging and regulates NAD(+) and NMN levels
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This study (species not specified) examined how CD38 is regulated during ageing and how its ecto-enzymatic activity affects NAD+ homeostasis, building on prior work showing CD38 knockout partially prevents NAD+ decline. The abstract reports that an increase in CD38 in white adipose tissue and liver during ageing was mediated by accumulation of CD38-positive immune cells, that inflammation increased CD38 and decreased NAD+, and that senescent cells and their secreted signals promoted accumulation of CD38-positive cells in white adipose tissue; ablation of senescent cells or their secretory phenotype decreased CD38 and partially reversed the NAD+ decline. Blocking CD38's ecto-enzymatic activity increased NAD+ through a nicotinamide mononucleotide (NMN)-dependent process.
Abstract
Decreased NAD+ levels have been shown to contribute to metabolic dysfunction during aging. NAD+ decline can be partially prevented by knockout of the enzyme CD38. However, it is not known how CD38 is regulated during aging, and how its ecto-enzymatic activity impacts NAD+ homeostasis. Here we show that an increase in CD38 in white adipose tissue (WAT) and the liver during aging is mediated by accumulation of CD38+ immune cells. Inflammation increases CD38 and decreases NAD+. In addition, senescent cells and their secreted signals promote accumulation of CD38+ cells in WAT, and ablation of senescent cells or their secretory phenotype decreases CD38, partially reversing NAD+ decline. Finally, blocking the ecto-enzymatic activity of CD38 can increase NAD+ through a nicotinamide mononucleotide (NMN)-dependent process. Our findings demonstrate that senescence-induced inflammation promotes accumulation of CD38 in immune cells that, through its ecto-enzymatic activity, decreases levels of NMN and NAD+.
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