ReviewEuropean journal of nutrition2023
Trimethylamine N-oxide: role in cell senescence and age-related diseases.
Review in European journal of nutrition, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 17 citations in OpenAlex.
- Gut Microbiota Modulation in CNS Disorders: Therapeutic Strategies and Implications for Drug Efficacy.Molecular neurobiology · 2026Review
- The complex of gut microbial metabolites and sex hormones in Alzheimer's disease.Seminars in immunopathology · 2026Review
- The gut microbiome and ageing trajectories: mechanisms and clinical implications.Nature reviews. Endocrinology · 2026Review
- TMAO Induced Kidney Aging by Activating ZBP1-Mediated Necroptosis.Physiological research · 2026Article
- Gut Microbiota-Derived Trimethylamine N-Oxide and NT-proBNP in Heart Failure: A Critical Review of Diagnostic and Prognostic Value.Biomedicines · 2026Review
- Sex-Specific Diet-Microbiota Interactions in Ageing: Implications for Healthy Longevity.Nutrients · 2025Review
- Adipocyte FMO3-derived TMAO induces WAT dysfunction and metabolic disorders by promoting inflammasome activation in ageing.Nature communications · 2025Article
- High-fat diet induces sarcopenic obesity in natural aging rats through the gut-trimethylamine N-oxide-muscle axis.Journal of advanced research · 2025Article
- Gut microbiota-driven neuroinflammation in Alzheimer's disease: from mechanisms to therapeutic opportunities.Frontiers in immunology · 2025Review
- Role of AMPK and Sirtuins in Aging Heart: Basic and Translational Aspects.Aging and disease · 2024Review
- Gut microbial metabolism in Alzheimer's disease and related dementias.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Review
- The Brain-Gut Axis, an Important Player in Alzheimer and Parkinson Disease: A Narrative Review.Journal of clinical medicine · 2024Review
- Therapeutics for neurodegenerative diseases by targeting the gut microbiome: from bench to bedside.Translational neurodegeneration · 2024Review
- Mendelian randomization analysis of the causal relationship between trimethylamine N-oxide and its precursors and Parkinson's disease.Archives of medical science : AMS · 2024Article
- The Role of the Gut Microbiome and Trimethylamine Oxide in Atherosclerosis and Age-Related Disease.International journal of molecular sciences · 2023Review
- Intestinal microbiota: a new perspective on delaying aging?Frontiers in microbiology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
introductionHayflick and Moorhead first demonstrated cell senescence as the irreversible growth arrest of cells after prolonged cultivation. Telomere shortening and oxidative stress are the fundamental mechanisms that drive cell senescence. Increasing studies have shown that TMAO is closely associated with cellular aging and age-related diseases. An emerging body of evidence from animal models, especially mice, has identified that TMAO contributes to senescence from multiple pathways and appears to accelerate many neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, the specific mechanism of how TMAO speeds aging is still not completely clear. MATERIAL AND
methodsIn this review, we summarize some key findings in TMAO, cell senescence, and age-related diseases. We focused particular attention on the potential mechanisms for clinical transformation to find ways to interfere with the aging process.
conclusionTMAO can accelerate cell senescence by causing mitochondrial damage, superoxide formation, and promoting the generation of pro-inflammatory factors.
Indexed as
Identifiers
What OpenQuestion holds
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.