ArticleEuropean journal of medical research2025
BRD4 silencing attenuates hemin-induced neuronal ferroptosis and inflammation via the H3K27ac-ATF3 axis in an in vitro model of cerebral hemorrhage.
Article in European journal of medical research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
backgroundIntracerebral hemorrhage (ICH), a subtype of hemorrhagic stroke, is associated with high morbidity and mortality. This study aimed to investigate the role and underlying mechanism of bromodomain and extraterminal domain protein 4 (BRD4) in neural injury following ICH.
methodsAn in vitro ICH model was established by treating SH-SY5Y cells with hemin. BRD4 and activating transcription factor 3 (ATF3) expression levels were altered using short hairpin RNA and pcDNA3.1 expression vectors. Cell viability and death were assessed using Cell Counting Kit-8 (CCK-8) and TdT-mediated dUTP nick-end labeling (TUNEL) assays. mRNA and protein expression levels were quantified by RT-qPCR and western blotting, respectively. Cytokine secretion was measured using enzyme-linked immunosorbent assay (ELISA) kits. Ferroptosis was evaluated based on levels of reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), and Fe
resultsBRD4 expression was upregulated in hemin-treated SH-SY5Y cells, and its knockdown repressed inflammation and ferroptosis induced by hemin. ATF3 expression was also elevated upon hemin stimulation and was identified as a downstream target of BRD4. Mechanistic studies revealed that BRD4 cooperated with H3K27ac to bind the ATF3 promoter, thereby promoting ATF3 transcription. Functional rescue experiments further demonstrated that ATF3 overexpression counteracted the inhibitory effects of BRD4 knockdown on hemin-induced inflammation and ferroptosis.
conclusionsBRD4 silencing alleviated hemin-induced neuronal ferroptosis and inflammation by regulating ATF3 transcription, suggesting that BRD4 inhibition may represent a potential therapeutic strategy for ICH.
Indexed as
Identifiers
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.