ArticleCell death & disease2020
Mithramycin selectively attenuates DNA-damage-induced neuronal cell death.
Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
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- Mechanistic insights and therapeutic interventions of mitochondrial quality control in chemotherapy-related cognitive impairment.Neoplasia (New York, N.Y.) · 2026Review
- Parthanatos drives cognitive decline in repeated brain trauma: MSC-derived exosomes as a novel therapeutic strategy.Frontiers in pharmacology · 2025Article
- AI-based classification of anticancer drugs reveals nucleolar condensation as a predictor of immunogenicity.Molecular cancer · 2024Article
- Neuron-targeted overexpression of caveolin-1 alleviates diabetes-associated cognitive dysfunction via regulating mitochondrial fission-mitophagy axis.Cell communication and signaling : CCS · 2023Article
- Cognitive adverse effects of chemotherapy and immunotherapy: are interventions within reach?Nature reviews. Neurology · 2022Review
- Traumatic Brain Injury Induces cGAS Activation and Type I Interferon Signaling in Aged Mice.Frontiers in immunology · 2021Article
- Protective Effects of Polydatin on Reproductive Injury Induced by Ionizing Radiation.Dose-response : a publication of International Hormesis SocietyArticle
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
DNA damage triggers cell death mechanisms contributing to neuronal loss and cognitive decline in neurological disorders, including traumatic brain injury (TBI), and as a side effect of chemotherapy. Mithramycin, which competitively targets chromatin-binding sites of specificity protein 1 (Sp1), was used to examine previously unexplored neuronal cell death regulatory mechanisms via rat primary neurons in vitro and after TBI in mice (males). In primary neurons exposed to DNA-damage-inducing chemotherapy drugs in vitro we showed that DNA breaks sequentially initiate DNA-damage responses, including phosphorylation of ATM, H
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Registered trials
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