ArticleOncotarget2017
Senoptosis: non-lethal DNA cleavage as a route to deep senescence.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 26 citations in OpenAlex.
- Exploring Stem Cell Based Senotherapeutic Strategies for Targeting Cellular Senescence in Brain Aging.Stem cell reviews and reports · 2026Review
- Induction of postmeiotic DNA double-strand breaks by the Pnu1 endonuclease inMolecular biology of the cell · 2025Article
- Metabolism and metabolomics in senescence, aging, and age-related diseases: a multiscale perspective.Frontiers of medicine · 2025Review
- Cellular senescence, neuroinflammation, and microRNAs: Possible interactions driving aging and neurodegeneration in the hippocampal neurogenic niche.Aging brain · 2025Review
- Anti-apoptosis effect of traditional Chinese medicine in the treatment of cerebral ischemia-reperfusion injury.Apoptosis : an international journal on programmed cell death · 2023Review
- Unraveling the effect of intra- and intercellular processes on acetaminophen-induced liver injury.NPJ systems biology and applications · 2022Article
- Comprehensive investigations of key mitochondrial metabolic changes in senescent human fibroblasts.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2022Article
- Mitochondrial dysfunction in cell senescence and aging.The Journal of clinical investigation · 2022Review
- Skin Aging, Cellular Senescence and Natural Polyphenols.International journal of molecular sciences · 2021Review
- Alternative Splicing of Human Telomerase Reverse Transcriptase (hTERT) and Its Implications in Physiological and Pathological Processes.Biomedicines · 2021Review
- Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence.Pharmacology & therapeutics · 2021Review
- Senescence-Induced Chemoresistance in Triple Negative Breast Cancer and Evolution-Based Treatment Strategies.Frontiers in oncology · 2021Review
- Regulation of the mitochondrial permeability transition pore and its effects on aging.Microbial cell (Graz, Austria) · 2020Article
- Pro- and anti-tumorigenic functions of the senescence-associated secretory phenotype.Expert opinion on therapeutic targets · 2019Review
- Review
- Article
- Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats.Journal of molecular neuroscience : MN · 2018Article
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
No grant is acknowledged in the PubMed record.
Abstract
DNA-damage-induced apoptosis and cellular senescence are perceived as two distinct cell fates. We found that after ionizing radiation (IR)-induced DNA damage the majority (up to 70 %) of senescent human diploid fibroblasts (HDFs) were subjected to controlled cleavage of DNA, resulting in the establishment of a viable and stable sub-G1 population, i.e. deeply senescent cells. We show that in senescent HDFs this DNA cleavage is triggered by modest loss of the mitochondrial membrane potential, which is not sufficient to activate caspases, but strong enough to release mitochondrial endonuclease G (EndoG). We demonstrate that upon γ-irradiation in HDFs EndoG translocates into the nucleus playing an essential role in the non-lethal cleavage of damaged DNA. Notably, the established sub-G1 cell population does not contribute to the senescence-associated secretory phenotype (SASP), however, it exhibits increased senescence-associated β-galactosidase activity. We show that EndoG knockdown causes an increase in DNA damage, indicating a role of this enzyme in DNA repair. Thus, we conclude that IR-induced deep senescence of HDFs exhibits features of both senescence, such as cell cycle arrest and viability, and apoptosis like reduced DNA content and no SASP, and, resembles uncomplete or stalled apoptosis, a phenomenon we term senoptosis.
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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.