ReviewThe FEBS journal2018
Nutrient sensing, growth and senescence.
Review in The FEBS journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 49 citations in OpenAlex.
- Senescent macrophages in tumor: phenotypes, roles, and interventions.Cell death & disease · 2025Review
- Senescence in the ageing skin: a new focus on mTORC1 and the lysosome.The FEBS journal · 2025Review
- Treating Metabolic Dysregulation and Senescence by Caloric Restriction: Killing Two Birds with One Stone?Antioxidants (Basel, Switzerland) · 2025Review
- Dissecting the Heterogeneity of Senescent Cells Through CITE-seq Integration.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Review
- MIS18A upregulation promotes cell viability, migration and tumor immune evasion in lung adenocarcinoma.Oncology letters · 2024Article
- Molecular mechanisms of aging and anti-aging strategies.Cell communication and signaling : CCS · 2024Review
- Review
- Underlying Mechanisms and Treatment of Cellular Senescence-Induced Biological Barrier Interruption and Related Diseases.Aging and disease · 2024Review
- Hepatic Global Transcriptomic Profiles of Holstein Cows According to Parity Reveal Age-Related Changes in Early Lactation.International journal of molecular sciences · 2023Article
- Palbociclib-Induced Cellular Senescence Is Modulated by the mTOR Complex 1 and Autophagy.International journal of molecular sciences · 2023Article
- TFEB-dependent lysosome biogenesis is required for senescence.The EMBO journal · 2023Article
- Technologies, strategies, and cautions when deconvoluting genome-wide association signals: FTO in focus.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2023Review
- Sex difference and immunosenescence affect transplantation outcomes.Frontiers in transplantation · 2023Review
- Nutritional Niches of Cancer Therapy-Induced Senescent Cells.Nutrients · 2022Article
- Nutritional components as mitigators of cellular senescence in organismal aging: a comprehensive review.Food science and biotechnology · 2022Review
- Periodontal microorganisms and Alzheimer disease - A causative relationship?Periodontology 2000 · 2022Review
- Aging conundrum: A perspective for ovarian aging.Frontiers in endocrinology · 2022Review
- Glutamine Availability Regulates the Development of Aging Mediated by mTOR Signaling and Autophagy.Frontiers in pharmacology · 2022Article
- An updated SYSCILIA gold standard (SCGSv2) of known ciliary genes, revealing the vast progress that has been made in the cilia research field.Molecular biology of the cell · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cell growth is dictated by a wide range of mitogenic signals, the amplitude and relative contribution of which vary throughout development, differentiation and in a tissue-specific manner. The ability to sense and appropriately respond to changes in mitogens is fundamental to control cell growth, and reduced responsiveness of nutrient sensing pathways is widely associated with human disease and ageing. Cellular senescence is an important tumour suppressor mechanism that is characterised by an irreversible exit from the cell cycle in response to replicative exhaustion or excessive DNA damage. Despite the fact that senescent cells can no longer divide, they remain metabolically active and display a range of pro-growth phenotypes that are supported in part by the mTORC1-autophagy signalling axis. As our understanding of the basic mechanisms of controlling mTORC1-autophagy activity and cell growth continues to expand, we are able to explore how changes in nutrient sensing contribute to the acquisition and maintenance of cellular senescence. Furthermore, while the protective effect of senescence to limit cellular transformation is clear, more recently, the age-related accumulation of these pro-inflammatory senescent cells has been shown to contribute to a decline in organismal fitness. We will further discuss whether dysregulation of nutrient sensing pathways can be targeted to promote senescent cell death which would have important implications for healthy ageing.
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.