Article: CD38 Inhibitor Reverses Age-Related NAD+ Decline and Metabolic Dysfunction: Preclinical Findings

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Mitochondrial Health Preclinical

CD38 Inhibitor Reverses Age-Related NAD+ Decline and Metabolic Dysfunction: Preclinical Findings

Synopsis

Aging is characterized by the development of metabolic dysfunction and frailty. Recent studies show that a reduction in nicotinamide adenine dinucleotide (NAD+) is a key factor for the development of age-associated metabolic decline. The enzyme CD38, which breaks down NAD+, plays a key role in this decline. Using a powerful, specific CD38 inhibitor called 78c, researchers reversed age-related NAD+ loss in mice and improved metabolic health markers such as glucose tolerance, muscle and heart function, and exercise ability. The benefits depended on NAD+ levels and were blocked if NAD+ synthesis was inhibited. Increased NAD+ activated longevity-related proteins (sirtuins, AMPK, PARPs) and suppressed pathways that harm health span (mTOR-S6K, ERK). Additionally, DNA damage linked to aging was reduced. This suggests targeting CD38 to maintain NAD+ is a promising way to prevent or reverse aging-related metabolic decline.

Journal

Cell Metabolism

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