ArticleApplied biochemistry and biotechnology2025
Mechanism of KDM4A in Regulating Microglial Polarization in Ischemic Stroke.
Article in Applied biochemistry and biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed.
- Inhibition of Astrocytic JMJD3 Attenuates Neuroinflammation-Mediated Blood-Brain Barrier Disruption and Improves Functional Recovery After Intracerebral Hemorrhage in Mice.Brain sciences · 2026Article
- The JMJD family histone demethylases: structure, mechanism of action, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- Targeting Epigenetics in Ischemic Stroke: From Mechanisms to Therapeutics.Current neuropharmacology · 2026Review
- Serum Hepatocyte-Derived Fibrinogen-Related Protein-1: A Novel Biomarker for Severity and Clinical Outcome in Acute Ischemic Stroke.Journal of inflammation research · 2026Article
- Association between circulating plasma CTRP3 levels and acute ischemic stroke: a systematic review and meta-analysis.Frontiers in neuroscience · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Microglia polarization plays important roles in inflammatory processes after ischemic stroke. This study aimed to explore the mechanism of lysine-specific histone demethylase 4 (KDM4A) in microglia polarization after ischemic stroke. The mouse model was established using middle cerebral artery occlusion/reperfusion (MCAO/R) and the cell model was established by oxygen-glucose deprivation/reperfusion (OGD/R). The neurological deficits and brain tissue injury were evaluated. The biomarkers of microglia were determined. Levels of KDM4A/mouse double minute-2 homolog (MDM2)/C1q/TNF-related protein-3 (CTRP3) were measured. Inflammatory cytokines were quantified. The impact of KDM4A on microglia polarization was assessed. The enrichment of KDM4A or histone 3 lysine 9 trimethylation (H3K9me3) on the MDM2 promoter was analyzed. The ubiquitination and protein levels of CTRP3 after MG132 and cycloheximide treatment were determined. Results showed that KDM4A and MDM2 were upregulated while CTRP3 was downregulated. KDM4A downregulation alleviated neurological dysfunction, rescued motor capacity, reduced inflammatory infiltration, suppressed microglia activation, and promoted M2 polarization. KDM4A inhibited the enrichment of H3K9me3 on the MDM2 promoter, increasing MDM2 expression and downregulating CTRP3 expression via ubiquitination and degradation. MDM2 overexpression or CTRP3 downregulation averted the promotive role of silencing KDM4A in microglia polarization. In conclusion, KDM4A promotes microglia polarization to aggravate ischemic stroke via the MDM2/CTRP3 axis.
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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.