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Therapeutic Effect of Nicotinamide Mononucleotide on Acute Kidney Injury Therapeutic Effect of Nicotinamide Mononucleotide on Acute Kidney Injury

The incidence and mortality of acute kidney injury (AKI) have increased year by year, and it has attracted more and more attention. Studies have shown that the levels of Sirt1 and NAD+ decrease with age. A decrease in NAD+ and Sirt1 in the kidneys of aged organisms leads to an increased susceptibility to AKI. Supplementation with nicotinamide mononucleotide protects mice from AKI induced by cisplatin, which can be used to inhibit DNA replication. The CAS number of nicotinamide mononucleotide is 1094-61-7. The mechanism by which NAD+/Sirt1 protects the kidney involves epigenetic regulation of the JNK pathway. In vitro, Sirt1 attenuates stress responses by modulating the JNK signaling pathway. Endogenous NAD+ is considered a potential therapeutic target for AKI in the elderly, and NMN is an excellent therapeutic strategy by supplementing NAD+.
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