ArticleFrontiers in public health2026
SIRT1 regulates dermal fibroblast senescence via impaired deacetylase function and mitochondrial dysfunction during skin aging induced by chronic oral cadmium exposure.
Article in Frontiers in public health, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- SIRT1 in Senescence: Mitochondria and Immune Crosstalk.Biology · 2026Review
- Running out the clock: Circadian rhythm dysfunction in cognitive disease.International review of neurobiology · 2026Review
- Agitation, Alzheimer's disease, and autophagy: mechanistic insights into aging pathways, gut microbiome, and artificial intelligence.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
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Abstract
Introduction: Skin aging is a complex, multifactorial biological process that can be significantly accelerated by environmental toxicants such as cadmium (Cd), a highly toxic and ubiquitous heavy metal. Although the broad cytotoxic impacts of Cd have been extensively reported, a comprehensive understanding of the precise molecular pathways underlying Cd-induced skin senescence is still lacking. In this study, we investigated the protective role of Sirtuin 1 (SIRT1), a highly conserved nicotinamide adenine dinucleotide (NAD Methods: To delineate the influence of SIRT1 on dermal aging, we established an Results: Our results demonstrate that Cd exposure elevates reactive oxygen species (ROS), disrupts mitochondrial integrity, and activates DNA damage responses, collectively driving cellular senescence. SIRT1 was shown to exert protective effects through the deacetylation of key substrates such as P53 and SOD2, thereby restoring redox balance and promoting DNA repair. The elevation of SIRT1 expression markedly mitigated mitochondrial impairments, senescent phenotypes, and apoptotic features triggered by Cd exposure. Conclusion: Our findings position SIRT1 as a crucial regulator of Cd-induced skin aging and suggest that targeting this deacetylase may provide a viable strategy to counteract skin degeneration caused by environmental insults.
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Registered trials
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