ArticleBMB reports2023
Fatty acid oxidation regulates cellular senescence by modulating the autophagy-SIRT1 axis.
Article in BMB reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- KU80 suppresses endonuclease G activity to preserve genomic integrity.The FEBS journal · 2026Article
- Novel applications of SIRT1 in Chronic Kidney Disease.Frontiers in medicine · 2026Review
- ApoA5-CIDEC axis regulates hepatic lipid metabolism, inflammation, and fibrosis in MASLD.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Beyond Bioenergetics: Emerging Roles of Mitochondrial Fatty Acid Oxidation in Stress Response and Aging.Cells · 2025Review
- Role of sirtuin 1 in depression‑induced coronary heart disease: Molecular pathways and therapeutic potential (Review).Biomedical reports · 2025Review
- Renal Fibrosis: SIRT1 Still of Value.Biomedicines · 2024Review
- The Roles of Caloric Restriction Mimetics in Central Nervous System Demyelination and Remyelination.Current issues in molecular biology · 2023Review
- SF3B4 Regulates Cellular Senescence and Suppresses Therapy-induced Senescence of Cancer Cells.Cancer genomics & proteomicsArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Senescence, a cellular process through which damaged or dysfunctional cells suppress the cell cycle, contributes to aging or age-related functional decline. Cell metabolism has been closely correlated with aging processes, and it has been widely recognized that metabolic changes underlie the cellular alterations that occur with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We found that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, increased formation of autophagosomes following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we found that inhibition of autophagy or enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence. [BMB Reports 2023; 56(12): 651-656].
Indexed as
Identifiers
37679295PMC10761749W4386468143What 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.