ArticleJournal of neuroinflammation2015
MicroRNA367 negatively regulates the inflammatory response of microglia by targeting IRAK4 in intracerebral hemorrhage.
Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- A Systematic Review of MicroRNAs in Hemorrhagic Neurovascular Disease: Cerebral Cavernous Malformations as a Paradigm.International journal of molecular sciences · 2025Pooled it
- Antimicrobial coated intracortical probes reduce invading microbe abundance and subsequent neuroinflammation.Biomaterials · 2026Article
- Modulating miRNA-367-3p Expression by Kaempferol Alleviates Experimental Autoimmune Encephalomyelitis: Targeting Fpn1-Dependent Ferroptosis and cAMP/CREB/CNTF Signaling.Neurochemical research · 2026Article
- Exosomal MicroRNA: an Effective Strategy for the Treatment of Intracerebral Hemorrhage.Molecular neurobiology · 2025Review
- Blood-Brain Barrier-Penetrating Nanocarriers Enable Microglial-Specific Drug Delivery in Hypothalamic Neuroinflammation.Advanced healthcare materials · 2025Article
- A Potential Role of EFR3A in Human Disease States.Biomolecules · 2025Review
- Molecular Pathogenesis of Ischemic and Hemorrhagic Strokes: Background and Therapeutic Approaches.International journal of molecular sciences · 2024Review
- Dysregulated expression of miR‑367 in disease development and its prospects as a therapeutic target and diagnostic biomarker (Review).Biomedical reports · 2023Review
- Non-Coding RNA in Microglia Activation and Neuroinflammation in Alzheimer's Disease.Journal of inflammation research · 2023Review
- Minor Changes for a Major Impact: A Review of Epigenetic Modifications in Cell-Based Therapies for Stroke.International journal of molecular sciences · 2022Review
- Interleukin-1 receptor-associated kinase 4 (IRAK4) in the nucleus accumbens regulates opioid-seeking behavior in male rats.Brain, behavior, and immunity · 2022Article
- Article
- MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy.Frontiers in immunology · 2022Review
- Effects of adenovirus-mediated knockdown of IRAK4 on synovitis in the osteoarthritis rabbit model.Arthritis research & therapy · 2021Article
- 1,4-Naphthoquinone Is a Potent Inhibitor of IRAK1 Kinases and the Production of Inflammatory Cytokines in THP-1 Differentiated Macrophages.ACS omega · 2021Article
- Preterm Intraventricular Hemorrhage-Induced Inflammatory Response in Human Choroid Plexus Epithelial Cells.International journal of molecular sciences · 2021Article
- New epigenetic players in stroke pathogenesis: From non-coding RNAs to exosomal non-coding RNAs.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- lncRNA MEG3 Downregulation Relieves Intracerebral Hemorrhage by Inhibiting Oxidative Stress and Inflammation in an miR-181b-Dependent Manner.Medical science monitor : international medical journal of experimental and clinical research · 2021Article
- Diagnostic and Prognostic Circulating MicroRNA in Acute Stroke: A Systematic and Bioinformatic Analysis of Current Evidence.Journal of stroke · 2021Review
- Mild hypothermia improves brain injury in rats with intracerebral hemorrhage by inhibiting IRAK2/NF-κB signaling pathway.Brain and behavior · 2021Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntracerebral hemorrhage (ICH) induces microglial activation and the release of inflammatory cytokines, leading to inflammation in the brain. IRAK4, an essential component of the MyD88-dependent pathway, activates subsets of divergent signaling pathways in inflammation.
methodsIn the experiment, microglia were stimulated with erythrocyte lysates, and then miR-367, IRAK4, NF-ĸB activation and downstream proinflammatory mediator production were analyzed. In addition, inflammation, brain edema, and neurological functions in ICH mice were also assessed.
resultsHere, we report that ICH downregulated miR-367 expression but upregulated IRAK4 expression in primary microglia. We also demonstrate that miR-367 suppressed IRAK4 expression by directly binding its 3'-untranslated region. MiR-367 inhibited NF-ĸB activation and downstream proinflammatory mediator production. Knocking down IRAK4 in microglia significantly decreased the IRAK4 expression and inhibited the NF-ĸB activation and the downstream production of proinflammatory mediators. In addition, our results indicate that miR-367 could inhibit expression of proinflammatory cytokines, reduce brain edema, and improve neurological functions in ICH mice.
conclusionsIn conclusion, our study demonstrates that miR-367/IRAK4 pathway plays an important role in microglial activation and neuroinflammation in ICH. Our finding also suggests that miR-367 might represent a potential therapeutic target for ICH.
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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.