ArticleCell death & disease2013
Mitochondrial DNA damage induces apoptosis in senescent cells.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.
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- Shikonin attenuates doxorubicin-induced myocardial senescence and fibrosis in association with improved redox and mitochondrial homeostasis.Molecular biology reports · 2026Article
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- Herpes simplex virus-thymidine kinase/ganciclovir suppressed the growth of lung adenocarcinoma cells accompanied by premature senescence.Translational cancer research · 2025Article
- The Role of Senescence in Experimental Periodontitis at the Causal Level: An in Vivo Study.Cells · 2025Article
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Revolutionizing Senescence Detection: Advancements from Traditional Methods to Cutting-Edge Techniques.Aging and disease · 2024Review
- Role of cellular senescence in inflammation and regeneration.Inflammation and regeneration · 2024Review
- Mitochondrial Dysfunction: A Key Player in Brain Aging and Diseases.Current issues in molecular biology · 2024Review
- Effects of Redox Homeostasis and Mitochondrial Damage on Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2023Review
- Generation of a p21 Reporter Mouse and Its Use to Identify and Eliminate p21International journal of molecular sciences · 2023Article
- Cigarette smoke induces mitochondrial DNA damage and activates cGAS-STING pathway: application to a biomarker for atherosclerosis.Clinical science (London, England : 1979) · 2023Article
- Neurotrophic effects of intermittent fasting, calorie restriction and exercise: a review and annotated bibliography.Frontiers in aging · 2023Review
- Efficacy and limitations of senolysis in atherosclerosis.Cardiovascular research · 2022Article
- Senescent hepatic stellate cells promote liver regeneration through IL-6 and ligands of CXCR2.JCI insight · 2022Article
- Article
- Fisetin as a Senotherapeutic Agent: Biopharmaceutical Properties and Crosstalk between Cell Senescence and Neuroprotection.Molecules (Basel, Switzerland) · 2022Review
- Association between single nucleotide polymorphism of rs1937 in TFAM gene and longevity among the elderly Chinese population: based on the CLHLS study.BMC geriatrics · 2022Article
- Translation of Cellular Senescence to Novel Therapeutics: Insights From Alternative Tools and Models.Frontiers in aging · 2022Review
- A guide to senolytic intervention in neurodegenerative disease.Mechanisms of ageing and development · 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
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Senescence is a cellular response to damage and stress. The senescence response prevents cancer by suppressing the proliferation of cells with a compromised genome and contributes to optimal wound healing in normal tissues. Persistent senescent cells are also thought to drive aging and age-associated pathologies through their secretion of inflammatory factors that modify the tissue microenvironment and alter the function of nearby normal or transformed cells. Understanding how senescent cells alter the microenvironment would be aided by the ability to induce or eliminate senescent cells at will in vivo. Here, we combine the use of the synthetic nucleoside analog ganciclovir (GCV) with herpes simplex virus thymidine kinase (HSVtk) activity to create or eliminate senescent human cells. We show that low concentrations of GCV induce senescence through the accumulation of nuclear DNA damage while higher concentrations of GCV, similar to those used in vivo, kill non-dividing senescent cells via mitochondrial DNA (mtDNA) damage and caspase-dependent apoptosis. Using this system, we effectively eliminated xenografted normal human senescent fibroblasts or induced senescence in human breast cancer cells in vivo. Thus, cellular senescence and mtDNA damage are outcomes of synthetic nucleoside analog treatment, indicating that the GCV-HSVtk combination can be used effectively to promote the targeted formation or eradication of senescent cells.
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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.