ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Nicotine Reprograms Aging-Related Metabolism and Protects Against Motor Decline in Mice.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Dibutyl phthalate induces sarcopenia via TNFα/TNFR1-mediated proteolytic and pyroptotic axes: evidence from NHANES and experimental models.Frontiers in immunology · 2026Article
- Complete nicotine biosynthesis reshapes the understanding of a classic alkaloid metabolic pathway.Frontiers in plant science · 2026Article
- Sympathetic-parasympathetic system deregulation theory of aging.npj aging · 2025Review
- Nicotine Reprograms Aging-Related Metabolism and Protects Against Motor Decline in Mice.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Correlation between smoking and delirium in patients with sepsis: A retrospective analysis utilizing the MIMIC database.Tobacco induced diseases · 2025Article
Corrections and comments
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Authors and funding
30 authors.
Funding
Abstract
The effects of nicotine on aging-related motor and cognitive decline remain controversial due to limited empirical evidence. Here, mice are permitted to orally consume nicotine over a 22-month period and observed attenuated motor decline without pathological alterations in major metabolism-related peripheral organs or immune system dysfunction. Multi-organ metabolomic profiling and network analysis of aged mice (24 months old) identified nicotine-responsive pathways related to glycolipid metabolism and energy homeostasis. Dynamic gut microbiota profiling via series expression miner-based longitudinal analysis reveals that nicotine consumption preserved microbiota composition and altered microbial-derived metabolites associated with the sphingolipid pathway, known to regulate age-related muscle dysfunction and sarcopenia. Assays in aged mice and C2C12 cells confirmed that nicotine regulates sphingolipid turnover, particularly via sphingomyelin synthases and neutral sphingomyelinases, to enhance nicotinamide adenine dinucleotide availability and energy metabolism. These metabolic adaptations correlated with reduced ceramide accumulation and improved motor function. Behavior-Metabolome Age (BMAge) score confirmed a biologically younger phenotype in the nicotine-treated mice. Together, these findings suggest that life-long oral nicotine consumption reprograms aging-associated metabolism through regulation of systemic sphingolipid homeostasis, conferring resilience against age-related motor decline.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.