Cure8 research brief
The study links macrophage CD38-driven NAD depletion to intestinal inflammation and shows that restoring NAD or blocking CD38 reduced disease in experimental colitis—suggesting a new metabolic target for IBD therapies.
Researchers in IBD immunometabolism, translational scientists, and clinicians following emerging therapeutic targets for inflammatory bowel disease.
This study (abstract) reports that NAD metabolism is disrupted in experimental colitis and that CD38, an enzyme that degrades NAD, is increased—particularly in infiltrating macrophages.
Restoring NAD levels with precursors (nicotinamide mononucleotide) or inhibiting CD38 reduced colitis severity in the experimental model, and myeloid-specific deletion of Cd38 preserved NAD and lessened inflammation.
The paper identifies a CD38–NAD axis in macrophages as a mechanistic link between altered cellular metabolism and intestinal inflammation and suggests CD38 as a potential therapeutic target for IBD. The findings come from preclinical laboratory models rather than human clinical trials.
Because the source content available here is the journal abstract, the summary is grounded in that abstract rather than a full peer-reviewed article text or clinical data. This brief describes what the abstract reports without implying clinical benefit has been shown in patients.
Findings are from experimental (preclinical) colitis models reported in the article abstract; clinical relevance in humans is not established.
Review the original publication for the complete reporting, methods, and context.
This Cure8 brief is based on source text from the linked article. Cure8 is informational only and is not a substitute for professional medical advice, diagnosis, or treatment.
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