Preclinical mechanistic study
Nicotinamide mononucleotide ameliorates adriamycin-induced renal damage by epigenetically suppressing the NMN/NAD consumers mediated by Twist2
Kazuhiro Hasegawa, Yusuke Sakamaki, Masanori Tamaki, Shu Wakino
Scientific Reports · 2022 · 12(1):13712
Study at a glance
- Design
- Randomized preclinical adriamycin-nephropathy mouse experiment with renal histology, biochemical and epigenetic assays, cultured podocyte experiments, and observational human-biopsy staining.
- Population or model
- Eight-week-old male BALB/c mice with adriamycin-induced focal segmental glomerulosclerosis-like injury; cultured renal cells and human biopsy specimens were used for supporting mechanistic observations.
- Sample size
- Main mouse groups: 12 per group; individual analyses generally used 6–20 observations per group
- Intervention
- Intraperitoneal NMN at 100, 300, or 500 mg/kg/day after adriamycin; the main regimen used 500 mg/kg/day for 14 days versus saline, with follow-up to day 28.
- Publication type
- Animal intervention study
- Evidence class
- preclinical-mechanistic
- Research area
- Renal injury and NAD+ metabolism
- Trial registration
- Not reported (animal study)
Study endpoints
- Urinary albumin-to-creatinine ratio, serum creatinine, creatinine clearance, and cholesterol
- Glomerulosclerosis, basement-membrane and podocyte measures
- Renal NAD+, NMN, and nicotinamide
- SIRT1, SIRT6, Claudin-1, Synaptopodin, Dnmt1, Nmnat1, PARP1, Twist2, and histone methylation
Plain-language summary
Key findings
Limitations
Funding and transparency
Funding
Scientific Research Fund of Japan MEXT (Grant 22K0835400).
Competing interests
The authors declared no competing interests.
HealthspanX observation
The main regimen was a high intraperitoneal dose in male mice and began around experimentally induced adriamycin injury; the human biopsy observations were not an NMN intervention.
Interpretive weight
Mechanistic context
The controlled mouse and cell experiments support a renal mechanism, but high-dose intraperitoneal treatment in one injury model cannot establish human efficacy or oral-product effects.
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