ArticleeLife2020
Opposing p53 and mTOR/AKT promote an in vivo switch from apoptosis to senescence upon telomere shortening in zebrafish.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 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
23 citing papers in PubMed, 46 citations in OpenAlex.
- Potential Probiotic Lacticaseibacillus rhamnosus NKU FL1-11 Prevents Aging-Related Oxidative Stress and Inflammation via mTOR and FoxO Signaling Pathways in Zebrafish.Probiotics and antimicrobial proteins · 2026Article
- cGAS-STING are responsible for premature aging of telomerase-deficient zebrafish.The EMBO journal · 2025Article
- Loss of Ten1 in mice induces telomere shortening and models human dyskeratosis congenita.Science advances · 2025Article
- Establishment and application of a zebrafish model of Werner syndrome identifies sapanisertib as a potential antiaging drug.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Genetic origins, regulators, and biomarkers of cellular senescence.Trends in genetics : TIG · 2024Review
- Cellular senescence in Alzheimer's disease: from physiology to pathology.Translational neurodegeneration · 2024Review
- Review
- Lack of telomerase reduces cancer incidence and increases lifespan of zebrafish tp53Scientific reports · 2024Article
- Senescence-associated ß-galactosidase staining over the lifespan differs in a short- and a long-lived fish species.European journal of histochemistry : EJH · 2024Article
- Article
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- Alterations in immune cell heterogeneities in the brain of aged zebrafish using single-cell resolution.Science China. Life sciences · 2023Article
- Gut-specific telomerase expression counteracts systemic aging in telomerase-deficient zebrafish.Nature aging · 2023Article
- Whole-mount Senescence-Associated Beta-Galactosidase (SA-β-GAL) Activity Detection Protocol for Adult Zebrafish.Bio-protocol · 2022Article
- Proteasome regulators in pancreatic cancer.World journal of gastrointestinal oncology · 2022Review
- Oridonin Delays Aging Through the AKT Signaling Pathway.Frontiers in pharmacology · 2022Article
- Cell senescence and malignant transformation in the inherited bone marrow failure syndromes: Overlapping pathophysiology with therapeutic implications.Seminars in hematology · 2022Review
- The right time for senescence.eLife · 2021Review
- Diverse roles of FOXO family members in gastric cancer.World journal of gastrointestinal oncology · 2021Review
- Translational Control during Cellular Senescence.Molecular and cellular biology · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Progressive telomere shortening during lifespan is associated with restriction of cell proliferation, genome instability and aging. Apoptosis and senescence are the two major outcomes upon irreversible cellular damage. Here, we show a transition of these two cell fates during aging of telomerase deficient zebrafish. In young telomerase mutants, proliferative tissues exhibit DNA damage and p53-dependent apoptosis, but no senescence. However, these tissues in older animals display loss of cellularity and senescence becomes predominant. Tissue alterations are accompanied by a pro-proliferative stimulus mediated by AKT signaling. Upon AKT activation, FoxO transcription factors are phosphorylated and translocated out of the nucleus. This results in reduced SOD2 expression causing an increase of ROS and mitochondrial dysfunction. These alterations induce p15/16 growth arrest and senescence. We propose that, upon telomere shortening, early apoptosis leads to cell depletion and insufficient compensatory proliferation. Following tissue damage, the mTOR/AKT is activated causing mitochondrial dysfunction and p15/16-dependent senescence.
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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.