ArticleMolecular medicine reports2019
D‑galactose induces astrocytic aging and contributes to astrocytoma progression and chemoresistance via cellular senescence.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- Neuroprotective effects of agomelatine in a D-galactose-induced hippocampal aging model.Toxicology reports · 2026Article
- Targeting CA2 Perineuronal Nets Restores Recognition Memory and Theta Oscillations in Aged Mice.Aging cell · 2025Article
- Article
- D-galactose Induces Senescence in Adult Mouse Neural Stem Cells by Imbalanced Oxidant and Antioxidant Activity and Differential Expression of Specific Hub Genes.Molecular neurobiology · 2025Article
- Mitigating Oxidative Stress and Promoting Cellular Longevity with Mushroom Extracts.Foods (Basel, Switzerland) · 2024Article
- Cellular senescence and metabolic reprogramming: Unraveling the intricate crosstalk in the immunosuppressive tumor microenvironment.Cancer communications (London, England) · 2024Review
- Interactions between oxidative stress and senescence in cancer: Mechanisms, therapeutic implications, and future perspectives.Redox biology · 2024Review
- Review
- Protective Effect of Curcumin on D-Galactose-Induced Senescence and Oxidative Stress in LLC-PK1 and HK-2 Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Intrinsic and Microenvironmental Drivers of Glioblastoma Invasion.International journal of molecular sciences · 2024Review
- Diosgenin alleviates D-galactose-induced oxidative stress in rats' brain and liver targeting aging and apoptotic marker genes.Frontiers in molecular biosciences · 2024Article
- Neuromodulatory effect of vardenafil on aluminium chloride/D-galactose induced Alzheimer's disease in rats: emphasis on amyloid-beta, p-tau, PI3K/Akt/p53 pathway, endoplasmic reticulum stress, and cellular senescence.Inflammopharmacology · 2023Article
- A systematic review for the development of Alzheimer's disease inFrontiers in aging neuroscience · 2023Article
- DDX58 expression promotes inflammation and growth arrest in Sertoli cells by stabilizing p65 mRNA in patients with Sertoli cell-only syndrome.Frontiers in immunology · 2023Article
- High fat diet-induced brain damaging effects through autophagy-mediated senescence, inflammation and apoptosis mitigated by ginsenoside F1-enhanced mixture.Journal of ginseng research · 2022Article
- Physiological and Pathological Ageing of Astrocytes in the Human Brain.Neurochemical research · 2021Review
- Cell aging related genes can be used to characterize clinical prognoses and further stratify diffuse gliomas.Scientific reports · 2021Article
- YAP prevents premature senescence of astrocytes and cognitive decline of Alzheimer's disease through regulating CDK6 signaling.Aging cell · 2021Article
- Increased exosome secretion in neurons aging in vitro by NPC1-mediated endosomal cholesterol buildup.Life science alliance · 2021Article
- Review
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The administration of D‑galactose triggers brain aging by poorly understood mechanisms. It is generally recognized that D‑galactose induces oxidative stress or affects protein modifications via receptors for advanced glycated end products in a variety of species. In the present study, we aimed to investigate the involvement of astrocytes in D‑galactose‑induced brain aging in vitro. We found that D‑galactose treatment significantly suppressed cell viability and induced cellular senescence. In addition, as of the accumulation of senescent cells, we proposed that the senescence‑associated secretory phenotype (SASP) can stimulate age‑related pathologies and chemoresistance in brain. Consistently, senescent astrocytic CRT cells induced by D‑galactose exhibited increases in the levels of IL‑6 and IL‑8 via NF‑κB activation, which are major SASP components and inflammatory cytokines. Conditioned medium prepared from senescent astrocytic CRT cells significantly promoted the viability of brain tumor cells (U373‑MG and N2a). Importantly, conditioned medium greatly suppressed the cytotoxicity of U373‑MG cells induced by temozolomide, and reduced the protein expression levels of neuron marker neuron‑specific class III β‑tubulin, but markedly increased the levels of c‑Myc in N2a cells. Thus, our findings demonstrated that D‑galactose treatment might mimic brain aging, and that D‑galactose could contribute to brain inflammation and tumor progression through inducing the accumulation of senescent‑secretory astrocytes.
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