ArticleThe Biochemical journal2003
Metabolic analysis of senescent human fibroblasts reveals a role for AMP in cellular senescence.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 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.
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Who cites it
113 citing papers in PubMed, 250 citations in OpenAlex.
- Folinic Acid Improves Healing of Diabetic Foot Ulcers.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyTrial
- Molecular mechanisms and recent advances in cellular senescence.Cell & bioscience · 2026Review
- Multi-tissue analysis identifies mitochondrial genes in chicken aging-induced productivity decline.Journal of animal science and biotechnology · 2026Article
- Review
- SREBP1-mediated lipogenesis promotes dedifferentiation and senescence of vascular smooth muscle cells through epigenetic remodeling.Nature communications · 2025Article
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Influence of Stress-Induced Senescence on the Secretome of Primary Mesenchymal Stromal Cells.Biomolecules · 2025Article
- Putrescine functions as a metabolic checkpoint in replication stress-induced senescence.Cellular and molecular life sciences : CMLS · 2025Article
- Emerging Radioligands as Tools to Track Multi-Organ Senescence.Diagnostics (Basel, Switzerland) · 2025Review
- Noncanonical function of Pannexin1 promotes cellular senescence and renal fibrosis post-acute kidney injury.Nature communications · 2025Article
- Cellular Models of Aging and Senescence.Cells · 2025Review
- P16-positive senescent cells promote DKD by the dysregulation of glycolysis and mitochondrial metabolism.Cell death discovery · 2025Article
- The Combination of Physiological and Transcriptomic Approaches Reveals New Insights into the Molecular Mechanisms ofInternational journal of molecular sciences · 2025Article
- Article
- Lactate in skin homeostasis: metabolism, skin barrier, and immunomodulation.Frontiers in immunology · 2025Review
- Cell senescence in cardiometabolic diseases.npj aging · 2024Review
- Metabolic fingerprinting by nuclear magnetic resonance of hepatocellular carcinoma cells during p53 reactivation-induced senescence.NMR in biomedicine · 2024Article
- Article
- The Role of Coenzyme Q10 in Skin Aging and Opportunities for Topical Intervention: A Review.The Journal of clinical and aesthetic dermatology · 2024Review
- The Role of Fibroblasts in Skin Homeostasis and Repair.Biomedicines · 2024Review
53 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is considered a major tumour-suppressor mechanism in mammals, and many oncogenic insults, such as the activation of the ras proto-oncogene, trigger initiation of the senescence programme. Although it was shown that activation of the senescence programme involves the up-regulation of cell-cycle regulators such as the inhibitors of cyclin-dependent kinases p16INK4A and p21CIP-1, the mechanisms underlying the senescence response remain to be resolved. In the case of stress-induced premature senescence, reactive oxygen species are considered important intermediates contributing to the phenotype. Moreover, distinct alterations of the cellular carbohydrate metabolism are known to contribute to oncogenic transformation, as is best documented for the phenomenon of aerobic glycolysis. These findings suggest that metabolic alterations are involved in tumourigenesis and tumour suppression; however, little is known about the metabolic pathways that contribute to these processes. Using the human fibroblast model of in vitro senescence, we analysed age-dependent changes in the cellular carbohydrate metabolism. Here we show that senescent fibroblasts enter into a metabolic imbalance, associated with a strong reduction in the levels of ribonucleotide triphosphates, including ATP, which are required for nucleotide biosynthesis and hence proliferation. ATP depletion in senescent fibroblasts is due to dysregulation of glycolytic enzymes, and finally leads to a drastic increase in cellular AMP, which is shown here to induce premature senescence. These results suggest that metabolic regulation plays an important role during cellular senescence and hence tumour suppression.
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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.