ArticleCell death and differentiation2017
Transient mitochondrial DNA double strand breaks in mice cause accelerated aging phenotypes in a ROS-dependent but p53/p21-independent manner.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 57 citations in OpenAlex.
- Changes in transposable elements expression in male and female mice liver throughout aging.GeroScience · 2026Article
- Impaired Complex I dysregulates neural/glial precursors and corpus callosum development revealing postnatal defects in Leigh syndrome mice.EMBO molecular medicine · 2026Article
- Redox-Immune Axis and Ozone Pollution: From Oxidative Stress to Thymic Involution and Neurodegeneration.Medical sciences (Basel, Switzerland) · 2025Review
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- Canagliflozin improves high-salt-induced aortic arteriosclerosis and premature aging in dahl salt-sensitive rats through the SIRT6/HIF-1 α signaling pathway.Molecular and cellular biochemistry · 2025Article
- Development and validation of AI-based automatic segmentation and measurement of thymus on chest CT scans.BMC medical imaging · 2025Article
- Divergent immediate and delayed effects of juvenile exposure to doxorubicin on the thymus in C57BL/6 mice.Scientific reports · 2025Article
- Revisiting the Role of Mitochondrial DNA Mutations in Aging: Bridging Theoretical Expectations with Empirical Observations.Aging and disease · 2025Review
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Molecular and cellular consequences of mitochondrial DNA double-stranded breaks.Human molecular genetics · 2024Review
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- DNA Double Strand Break and Response Fluorescent Assays: Choices and Interpretation.International journal of molecular sciences · 2024Review
- Interaction effect of mutations in the genes (piwi and aub) of the Argonaute family and hobo transposons on the integral survival parameters of Drosophila melanogaster.Biogerontology · 2024Article
- Review
- Mitochondrial DNA damage as driver of cellular outcomes.American journal of physiology. Cell physiology · 2022Review
- Mitochondrial Dysfunction in Alzheimer's Disease: Opportunities for Drug Development.Current neuropharmacology · 2022Article
- Mitochondrial genomic integrity and the nuclear epigenome in health and disease.Frontiers in endocrinology · 2022Article
- Sevoflurane Improves Hemorrhagic Shock and Resuscitation-Induced Cognitive Impairments and Mitochondrial Dysfunctions through SIRT1-Mediated Autophagy.Oxidative medicine and cellular longevity · 2022Article
- Hyperphosphatemia-Induced Oxidant/Antioxidant Imbalance Impairs Vascular Relaxation and Induces Inflammation and Fibrosis in Old Mice.Antioxidants (Basel, Switzerland) · 2021Article
- Altered Induction of Reactive Oxygen Species by X-rays in Hematopoietic Cells of C57BL/6-Tg (CAG-EGFP) Mice.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
We observed that the transient induction of mtDNA double strand breaks (DSBs) in cultured cells led to activation of cell cycle arrest proteins (p21/p53 pathway) and decreased cell growth, mediated through reactive oxygen species (ROS). To investigate this process in vivo we developed a mouse model where we could transiently induce mtDNA DSBs ubiquitously. This transient mtDNA damage in mice caused an accelerated aging phenotype, preferentially affecting proliferating tissues. One of the earliest phenotypes was accelerated thymus shrinkage by apoptosis and differentiation into adipose tissue, mimicking age-related thymic involution. This phenotype was accompanied by increased ROS and activation of cell cycle arrest proteins. Treatment with antioxidants improved the phenotype but the knocking out of p21 or p53 did not. Our results demonstrate that transient mtDNA DSBs can accelerate aging of certain tissues by increasing ROS. Surprisingly, this mtDNA DSB-associated senescence phenotype does not require p21/p53, even if this pathway is activated in the process.
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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.