Nicotinamide Mononucleotide Decreases Secretion Of Proinflammatory Cytokines Via The NAD + /Sirt1/P65 Axis
As we age, our cells can enter a state called senescence, where they stop dividing but remain active, often releasing harmful inflammatory substances. This process, known as the senescence-associated secretory phenotype (SASP), contributes to aging and various chronic diseases. Scientists are actively searching for compounds, called senomorphics, that can block this harmful inflammatory release. This research highlights a promising molecule called nicotinamide mononucleotide, or NMN. It was discovered that NMN efficiently reduces the secretion of these inflammatory signals from senescent cells. The mechanism behind this involves NMN significantly boosting levels of a vital molecule called NAD+ within these aging cells. This increase in NAD+ then activates a protein known as SIRT1, which plays a crucial role in cellular health and longevity. Activated SIRT1, in turn, modifies another protein called p65 by removing a specific chemical tag (acetylation). This modification suppresses the activity of p65, which is a key regulator of inflammation. By inhibiting p65, NMN effectively reduces the production and release of proinflammatory substances. These findings suggest that NMN could be a valuable senomorphic, offering a new approach to combat age-related inflammation and its associated health issues.
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