Nicotinamide mononucleotide ameliorates adriamycin-induced renal damage by epigenetically suppressing the NMN/NAD consumers mediated by Twist2.
Level 5 - mechanism / opinion, no new human data
Preclinical animal model (BALB/c mice) with no human clinical data
PubMed 35962139 · doi:10.1038/s41598-022-18147-2
What was done
Researchers evaluated the therapeutic effects and epigenetic mechanisms of nicotinamide mononucleotide (NMN) in 8-week-old BALB/c mice with adriamycin (ADR)-induced focal segmental glomerulosclerosis (FSGS). Mice received transient daily NMN administration for 14 consecutive days following ADR or saline control exposure. The study assessed urinary albumin excretion, renal histopathology (glomerulosclerosis), kidney NAD+ concentrations, and the expression and epigenetic regulation of Sirt1, Claudin-1, Dnmt1, Nmnat1, and PARP1.
What was found
The abstract reports directional effects without numerical values or confidence intervals: - NMN alleviated the elevated urinary albumin excretion and mitigated glomerulosclerosis in ADR-treated mice. - NMN treatment restored reduced Sirt1 expression, decreased elevated Claudin-1 expression, and increased NAD+ concentration in kidney tissue. - NMN improved histone methylation and Dnmt1 expression levels, which epigenetically repressed Nmnat1 and PARP1 expression.
Why it matters
This study identifies an epigenetic mechanism where NMN upregulates Sirt1 and suppresses NAD-consuming enzymes, suggesting a mechanistic target for podocyte and renal protection in focal glomerulosclerosis.
Limits
The study is restricted to an acute chemical injury (adriamycin) mouse model, which does not fully capture the complexity and chronicity of human FSGS. The abstract does not report sample sizes (n), dosing concentrations, exact numerical data, effect sizes, or long-term safety and efficacy outcomes.
Cited by
- supports Nicotinamide mononucleotide (NMN) alters the epigenome and modulates the immune system.