Nicotinamide reduced skin photoaging markers in mice by delaying cellular senescence
In mice, nicotinamide supplementation was reported to improve skin photoaging, restore skin barrier proteins and collagen I, lower senescence markers and suppress SASP factors. This is an abstract of animal and multi-omics work; it does not show human benefit. [1]
Automatic summary · not editorially reviewed
The key findings
Multi-omics analysis suggested insufficient nicotinamide metabolism may be associated with decreased NAD synthesis during skin aging. [1]
In mice, NAM supplementation was reported to ameliorate skin photoaging and restore barrier proteins and collagen I while lowering senescence markers. [1]
NAM was also found to suppress expression of senescence-associated secretory phenotype factors in skin photoaging. [1]
The source at a glance
- Study type / format
- Animal study reported in an abstract
- Population / context
- Mice with skin photoaging; multi-omics analysis of skin aging
- Summary based on
- Study abstract
- Original publication
- June 27, 2026
Nicotinamide metabolism and NAD in aging mouse skin
The abstract describes nicotinamide (NAM) as a precursor of nicotinamide adenine dinucleotide (NAD) and notes that NAM supplementation has shown benefits for cellular senescence. The authors state that multi-omics analysis revealed insufficient nicotinamide metabolism may be associated with decreased NAD synthesis during skin aging. They add that the mechanism by which NAM improves skin photoaging remained unclear, which framed the study.
Supporting source [1]
Mice: barrier proteins, collagen I and senescence markers
The authors report that NAM had an ameliorating effect on skin photoaging in mice. Supplementation restored expression of salvage-pathway enzymes and NAD consumers. It also restored skin barrier-related proteins (ZO1 and E-cadherin) and collagen I, while reducing expression of senescence markers (γ-H2AX, p53 and p21). Separately, NAM was found to suppress expression of senescence-associated secretory phenotype (SASP) factors in skin photoaging. The authors describe a dual role: delaying cellular senescence and suppressing SASP.
Supporting source [1]
Abstract-only animal evidence, not human lifespan data
These findings come from an abstract about mice and multi-omics analysis; the full text was not reviewed. The abstract reports marker expression and does not describe sample sizes, follow-up duration or a human comparison. Associations between NAM and these markers do not establish cause in people, and results in mice are not evidence of human lifespan or skin benefits.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Findings are from mice and multi-omics analysis, with no reported sample sizes, follow-up or human outcomes. Marker changes do not show causation or human lifespan benefit.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Tang XY, Lu KJ, Zhu R, Gao Y, Wei DY, Zhang XY, Ma YC, Wang FF, Zou CG. · europepmc.org · June 27, 2026