ArticleArchives of biochemistry and biophysics2017
Reciprocal regulation of acetyl-CoA carboxylase 1 and senescence in human fibroblasts involves oxidant mediated p38 MAPK activation.
Article in Archives of biochemistry and biophysics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Review
- Fatty acid synthesis therapy-induced senescence (FASTIS) in cancer cells.Cell death & disease · 2026Article
- Delta-9 desaturase reduction in gastrointestinal cells induced to senescence by doxorubicin.FEBS open bio · 2025Article
- Redox metabolism in cell senescence: focusing on contributions from the metabolomic field.Frontiers in molecular biosciences · 2025Review
- Cell-cell interactions mediating primary and metastatic breast cancer dormancy.Cancer metastasis reviews · 2024Review
- Losmapimod ameliorates doxorubicin-induced cardiotoxicity through attenuating senescence and inflammatory pathways.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Initial Phase of Anthracycline Cardiotoxicity Involves Cardiac Fibroblasts Activation and Metabolic Switch.Cancers · 2023Article
- Involvement of ACACA (acetyl-CoA carboxylase α) in the lung pre-metastatic niche formation in breast cancer by senescence phenotypic conversion in fibroblasts.Cellular oncology (Dordrecht, Netherlands) · 2023Article
- Curcumin supplementation increases longevity and antioxidant capacity inFrontiers in pharmacology · 2023Article
- Impact of Exercise and Aging on Mitochondrial Homeostasis in Skeletal Muscle: Roles of ROS and Epigenetics.Cells · 2022Review
- Skin Aging, Cellular Senescence and Natural Polyphenols.International journal of molecular sciences · 2021Review
- Lipid Players of Cellular Senescence.Metabolites · 2020Review
- FASN activity is important for the initial stages of the induction of senescence.Cell death & disease · 2019Article
- Oxidative Stress and Cellular Response to Doxorubicin: A Common Factor in the Complex Milieu of Anthracycline Cardiotoxicity.Oxidative medicine and cellular longevity · 2017Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
We sought to explore the fate of the fatty acid synthesis pathway in human fibroblasts exposed to DNA damaging agents capable of inducing senescence, a state of irreversible growth arrest. Induction of premature senescence by doxorubicin or hydrogen peroxide led to a decrease in protein and mRNA levels of acetyl-CoA carboxylase 1 (ACC1), the enzyme that catalyzes the rate-limiting step in fatty-acid biosynthesis. ACC1 decay accompanied the activation of the DNA damage response (DDR), and resulted in decreased lipid synthesis. A reduction in protein and mRNA levels of ACC1 and in lipid synthesis was also observed in human primary fibroblasts that underwent replicative senescence. We also explored the consequences of inhibiting fatty acid synthesis in proliferating non-transformed cells. Using shRNA technology, we knocked down ACC1 in human fibroblasts. Interestingly, this metabolic perturbation was sufficient to arrest proliferation and trigger the appearance of several markers of the DDR and increase senescence associated β-galactosidase activity. Reactive oxygen species and p38 mitogen activated protein kinase phosphorylation participated in the induction of senescence. Similar results were obtained upon silencing of fatty acid synthase (FAS) expression. Together our results point towards a tight coordination of fatty acid synthesis and cell proliferation in human fibroblasts.
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