NMN in D-gal-aged mouse C2C12 skeletal muscle cells: a cell study
In mouse C2C12 skeletal muscle cells made senescent with D-galactose, NMN treatment reduced reactive oxygen species, improved myotube formation and lowered several senescence-associated markers. This is a cell-culture abstract, not evidence of human benefit. [1]
Automatic summary · not editorially reviewed
The key findings
The study used D-galactose to create a senescence model in mouse C2C12 skeletal muscle cells. [1]
NMN treatment was associated with increased myotube formation and higher myosin heavy chain expression in aged C2C12 cells. [1]
NMN reduced reactive oxygen species in aged myoblasts and myotubes and lowered several senescence-associated markers. [1]
The source at a glance
- Study type / format
- In vitro cell-culture study (abstract)
- Population / context
- Mouse C2C12 skeletal muscle cells (myoblasts and myotubes) in a D-galactose senescence model
- Summary based on
- Study abstract
- Original publication
- September 22, 2026
D-galactose senescence model in mouse C2C12 cells
The authors note that skeletal muscle loses mass, strength and function during aging, and that NMN, a precursor of nicotinamide adenine dinucleotide (NAD), has been discussed for aging-associated diseases. They write that protective effects of NMN against skeletal muscle cell senescence are not yet fully clarified. To study this, they used D-galactose to establish a senescence model in mouse C2C12 skeletal muscle cells.
Supporting source [1]
NMN effects on aged myoblasts and myotubes
Aged C2C12 cells showed a significant impairment in differentiation capacity, which NMN treatment ameliorated, with increased myotube formation and higher myosin heavy chain expression. NMN significantly decreased reactive oxygen species in both aged myoblasts and myotubes. In aged myotubes, NMN downregulated mRNA of Trp53, PARPs and IL-1α, and attenuated the elevated p53 and IL-1β protein signals seen by immunofluorescence.
Supporting source [1]
Cell-culture scope of the NMN findings
The authors conclude that NMN attenuates D-galactose-induced reactive oxygen species accumulation, enhances myotube formation and downregulates several senescence-associated molecules. They call NMN a promising therapeutic agent for mitigating skeletal muscle cell aging. These are results in a mouse cell line under an induced senescence model; the abstract reports no animals, no human participants and no clinical outcomes.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings come from a mouse C2C12 cell line in a D-galactose-induced senescence model, with no animals, humans or clinical outcomes reported. The abstract gives no sample sizes, replication details or statistical uncertainty. The suggested therapeutic promise is not established for people.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Mi J, Wang C, Gu H, Wang M, Zhang W, Zhou Q, Zhang Y, Pan J, Yu L. · europepmc.org · September 22, 2026