NMN Ameliorates Doxorubicin-induced Kidney Injury

Recently, a new study evaluated the renoprotective effect of preemptive short-term NMN treatment on ADR-induced FSGS mice. The results suggest that NAD+ and Sirt1 deficiency contribute to susceptibility to kidney injury. Short-term NMN treatment rescued FSGS from podocyte damage by restoring renal NAD+ concentrations, even after treatment discontinuation. In addition, the study observed long-term effects on NAD+ metabolite kinetics after treatment, suggesting a legacy effect of Sirt1 reactivation.

In the present study, administration of NMN ameliorated renal injury both functionally and histologically in a mouse model of ADR-induced nephropathy. NMN maintained NAD+ levels and altered expression levels of Sirt1, Nampt, and Nmnat1 in the kidneys of ADR-treated mice. These changes were pronounced and persistent even after cessation of short-term NMN therapy, thus indicating that the effects of this treatment regimen were sustained. This study provides proof-of-concept for brief, short-term administration of NMN as an effective treatment for proteinuric nephropathy in the FSGS model.

NMN treatment for 14 days resulted in a sustained reduction in proteinuria in FSGS and improved histological changes such as foot process disappearance and glomerulosclerosis. We have previously shown that Sirt1 reduction in podocytes epigenetically upregulates levels of Claudin-1 (activated by Dnmt1) and reduces levels of Synaptopodin, subsequently leading to foot process loss and proteinuria. In addition, the expression levels of H3K9me2 and DNMT1 were lower in the glomeruli of ADR mice. NMN ameliorated these adverse changes, even after treatment discontinuation.

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