ArticleScientific reports2016
Restriction of protein synthesis abolishes senescence features at cellular and organismal levels.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
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- Aging clocks delineate neuron types vulnerable or resilient to neurodegeneration and identify neuroprotective interventions.Nature aging · 2026Article
- Stress-dependent growth in breast cancer arises from a mechano-osmotic coupling and cell-sizing checkpoint.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Interplay Between Ribosomal Gene Deficiency and Calorie Restriction in Shaping Yeast Biosynthetic Capacity.Cells · 2025Article
- Astrocytes as Metabolic Sensors Orchestrating Energy-Driven Brain Vulnerability in Alzheimer's Disease.Journal of neurochemistry · 2025Review
- Eukaryotic Elongation Factor 2 Kinase EFK-1/eEF2K promotes starvation resistance by preventing oxidative damage in C. elegans.Nature communications · 2025Article
- The brain-body energy conservation model of aging.Nature aging · 2024Review
- Article
- In-vivo screening implicates endoribonuclease Regnase-1 in modulating senescence-associated lysosomal changes.GeroScience · 2024Article
- Reducing the metabolic burden of rRNA synthesis promotes healthy longevity in Caenorhabditis elegans.Nature communications · 2024Article
- Stress-Induced Eukaryotic Translational Regulatory Mechanisms.Journal of clinical and medical sciences · 2024Article
- Proteostasis is differentially modulated by inhibition of translation initiation or elongation.eLife · 2023Article
- Early-adulthood spike in protein translation drives aging via juvenile hormone/germline signaling.Nature communications · 2023Article
- OxPhos defects cause hypermetabolism and reduce lifespan in cells and in patients with mitochondrial diseases.Communications biology · 2023Article
- Protein translation paradox: Implications in translational regulation of aging.Frontiers in cell and developmental biology · 2023Review
- G-quadruplexes and associated proteins in aging and Alzheimer's disease.Frontiers in aging · 2023Review
- Nutritional components as mitigators of cellular senescence in organismal aging: a comprehensive review.Food science and biotechnology · 2022Review
- Targeting tumor cell senescence and polyploidy as potential therapeutic strategies.Seminars in cancer biology · 2022Review
- Acceleration of ageing via disturbing mTOR-regulated proteostasis by a new ageing-associated gene PC4.Aging cell · 2021Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence or its equivalence is induced by treatment of cells with an appropriate inducer of senescence in various cell types. Mild restriction of cytoplasmic protein synthesis prevented induction of all aspects of cellular senescence in normal and tumor-derived human cells. It allowed the cells to continuously grow with no sign of senescent features in the presence of various inducers. It also delayed replicative senescence in normal human fibroblasts. Moreover, it allowed for growth of the cells that had entered a senescent state. When adult worms of the nematode C. elegans were grown under protein-restricted conditions, their average and maximal lifespans were significantly extended. These results suggest that accumulation of cytoplasmic proteins due to imbalance in macromolecule synthesis is a fundamental cause of cellular senescence.
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