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Studies have found that protecting skin cells from UV damage depends on the synthesis of NMN.

Studies have shown that maintaining NAD+ levels is critical for the survival of skin cells in response to UV damage. Tsuji-Naito and his colleagues from the laboratory of DHC in Japan published a study in the Journal of Photochemistry and Photobiology, which showed that UV damage activates NAD+ synthesis and NAD+ depletion enzymes. This is a balancing act that determines The survival or dysfunction of human skin cells. They showed that in a tug-of-war match, ultraviolet radiation activates nicotinamide phosphoribosyltransferase (NAMPT) to produce NAD+ precursor nicotinamide mononucleotide (NMN) and activates the NAD+-consuming enzyme poly ADP ribose polymerase (PARP) . If there are obstacles to NAD+ synthesis during this balancing process, PARP will severely deplete NAD+ levels, leading to stagnant skin cell proliferation and dysfunction.

Interestingly, preventing NAMPT from producing NAD+ allows PARP to excrete NAD+, but supplementing NAD+ precursor NMN (100 µM) or nicotinamide riboside (NR; 50 µM) can restore the ability of cells to recover from UV damage.