Fixing Imbalanced NAD Metabolism Reduces Effects of Telomere Dysfunction: Preclinical Findings
Synopsis
Short telomeres cause diseases like dyskeratosis congenita (DC), which lack effective treatments. This study found that cells from DC patients and telomerase-deficient mice have low NAD+ levels and an imbalance in enzymes controlling NAD+ metabolism. These changes led to problems with telomere damage, mitochondrial function, and cell aging. Supplementing with nicotinamide riboside (NR) or inhibiting an enzyme that breaks down NAD+ (CD38) restored NAD+ balance and improved cellular defects. This shows that NAD+ dysregulation is a key factor in telomere diseases and that targeting NAD+ metabolism could offer new treatments.
Journal
The EMBO Journal