ArticleBiomolecules & therapeutics2019
Etoposide Induces Mitochondrial Dysfunction and Cellular Senescence in Primary Cultured Rat Astrocytes.
Article in Biomolecules & therapeutics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 43 citations in OpenAlex.
- Distinct roles of COPI proteins attenuated in cell senescence.Science advances · 2026Article
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- Immunosenescence in Human Disease: Mechanistic Insights and Therapeutic Opportunities.Biomolecules & therapeutics · 2026Review
- Inflammation Affects the Osteogenic Differentiation of Aged Periodontal Ligament Cells via NF-κB/FOXO3a/c-JUN Signalling.Journal of periodontal research · 2026Article
- Senescent Astrocytes: A New Player in Brain Aging and Cognitive Decline.Brain sciences · 2026Review
- Mitochondrial regulation of cellular senescence heterogeneity.Frontiers in cell and developmental biology · 2026Review
- Complement pathway dysregulation and astrocyte alterations in Down syndrome: evidence from postmortem brain tissue and iPSC-derived astrocytes.Acta neuropathologica communications · 2025Article
- RNA G-quadruplex (rG4) exacerbates cellular senescence by mediating ribosome pausing.Protein & cell · 2025Article
- Article
- Doxorubicin Induces a Senescent Phenotype in Murine and Human Astrocytes.Journal of neurochemistry · 2025Article
- Hyperoxia-induced senescence in fetal airway smooth muscle cells: role of mitochondrial reactive oxygen species and endoplasmic reticulum stress.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Article
- Regulatory Network Inference of Induced Senescent Midbrain Cell Types Reveals Cell Type-Specific Senescence-Associated Transcriptional Regulators.bioRxiv : the preprint server for biology · 2025Article
- Comprehensive Cellular Senescence Evaluation to Aid Targeted Therapies.Research (Washington, D.C.) · 2025Article
- Development of Calcium-Dependent Phospholipase A2 Inhibitors to Target Cellular Senescence and Oxidative Stress in Neurodegenerative Diseases.Antioxidants & redox signaling · 2024Review
- Dental dysplasia in childhood cancer survivors: a case series of permanent tooth abnormalities.Oral and maxillofacial surgery · 2024Article
- Signal-Sustained Imaging of Mitophagy with an Enzyme-Activatable Metabolic Lipid Labeling Probe.Autophagy · 2024Article
- A Pro-Inflammatory Stimulus versus Extensive Passaging of DITNC1 Astrocyte Cultures as Models to Study Astrogliosis.International journal of molecular sciences · 2024Article
- Senescence in the bone marrow microenvironment: A driver in development of therapy-related myeloid neoplasms.Journal of bone oncology · 2024Article
- Targeting senescent cells with NKG2D-CAR T cells.Cell death discovery · 2024Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Brain aging is an inevitable process characterized by structural and functional changes and is a major risk factor for neurodegenerative diseases. Most brain aging studies are focused on neurons and less on astrocytes which are the most abundant cells in the brain known to be in charge of various functions including the maintenance of brain physical formation, ion homeostasis, and secretion of various extracellular matrix proteins. Altered mitochondrial dynamics, defective mitophagy or mitochondrial damages are causative factors of mitochondrial dysfunction, which is linked to age-related disorders. Etoposide is an anti-cancer reagent which can induce DNA stress and cellular senescence of cancer cell lines. In this study, we investigated whether etoposide induces senescence and functional alterations in cultured rat astrocytes. Senescence-associated β-galactosidase (SA-β-gal) activity was used as a cellular senescence marker. The results indicated that etoposide-treated astrocytes showed cellular senescence phenotypes including increased SA-β-gal-positive cells number, increased nuclear size and increased senescence-associated secretory phenotypes (SASP) such as IL-6. We also observed a decreased expression of cell cycle markers, including Phospho- Histone H3/Histone H3 and CDK2, and dysregulation of cellular functions based on wound-healing, neuronal protection, and phagocytosis assays. Finally, mitochondrial dysfunction was noted through the determination of mitochondrial membrane potential using tetramethylrhodamine methyl ester (TMRM) and the measurement of mitochondrial oxygen consumption rate (OCR). These data suggest that etoposide can induce cellular senescence and mitochondrial dysfunction in astrocytes which may have implications in brain aging and neurodegenerative conditions.
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