A Targeting Senescence and Recycling Intracellular Nicotinamide Adenine Dinucleotide Strategy for Attenuation of Senescence-Associated Phenotypes

Sep 5, 2025ACS nano

A Strategy to Reduce Aging Signs by Targeting Cell Aging and Recycling a Key Cellular Energy Molecule

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Abstract

The Cu-NAD@CM system can target senescent cells and restore NAD levels.

Cellular senescence is linked to aging and age-related diseases.
Nicotinamide adenine dinucleotide (NAD) is associated with cellular senescence but faces clinical application challenges.
The Cu-NAD@CM system was developed to improve the targeting and recycling of NAD in senescent cells.
This system inhibits the expression of senescence-associated secretory phenotype (SASP).
Evidence suggests potential therapeutic benefits in managing atherosclerosis and in mouse models of induced senescence.

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Cellular senescence is a critical factor in organismal aging and age-related diseases. Nicotinamide adenine dinucleotide (NAD) has been shown to be closely related to the cellular senescence process and holds potential as a senotherapeutic agent. However, its clinical application has been hindered by challenges such as its inability to be directly absorbed by cells, instability, and lack of targeting specificity. To address these issues, a senescent cell targeting and intracellular NADrecycling strategy for attenuation of senescence-associated phenotypes has been developed. As a proof of concept, we demonstrate that the Cu-NAD@CM system can target and recognize senescent cells while restoring the NADH to NADcycle and inhibiting senescence-associated secretory phenotype (SASP) expression. Our study reveals the significant therapeutic potential of the Cu-NAD@CM system in managing atherosclerosis (a disease involving multiple senescent cell types) and in doxorubicin-induced and d-galactose-induced senescent mouse models. + + +

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A Targeting Senescence and Recycling Intracellular Nicotinamide Adenine Dinucleotide Strategy for Attenuation of Senescence-Associated Phenotypes

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