ArticleMetabolic brain disease2022
miR-25-3p ameliorates SAE by targeting the TLR4/NLRP3 axis.
Article in Metabolic brain disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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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.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Inflammatory Changes after Medical Suppression of Suspected Endometriosis for Implantation Failure: Preliminary Results.International journal of molecular sciences · 2024Trial
- Circulating miRNAs as Biomarkers of Tick-Borne Encephalitis Severity: Association with Cytokine Profile in Febrile, Meningeal, and Encephalitic Forms.International journal of molecular sciences · 2026Article
- Inhibition of miR-25-3p Alleviates Neuroinflammation in Alzheimer's Disease By Targeting ADAM10.Molecular neurobiology · 2026Article
- Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy.International journal of molecular sciences · 2026Review
- Role of the intestinal microbiota in sepsis-associated encephalopathy.Burns & trauma · 2026Review
- OGT-Mediated O-GlcNAcylation of ATF2 Protects Against Sepsis-Associated Encephalopathy by Inhibiting Microglial Pyroptosis.Neuroscience bulletin · 2025Article
- Common and distinct circulating microRNAs in four neurovascular disorders.Biochemistry and biophysics reports · 2025Article
- Exosomes and microRNA - a new form of remote and bidirectional neuroimmunomodulation?Neuroimmunomodulation · 2025Review
- 17(R)-Resolvin D1 protects against sickle cell-related inflammatory cardiomyopathy in humanized mice.Blood · 2025Article
- Short-term exposure to particulate matter triggers a selective alteration of plasma extracellular vesicle-packaged miRNAs in a mouse model of multiple sclerosis.Frontiers in immunology · 2025Article
- Sepsis-associated encephalopathy: Autophagy and miRNAs regulate microglial activation.Physiological reports · 2024Review
- Inflammasomes in neurological disorders - mechanisms and therapeutic potential.Nature reviews. Neurology · 2024Review
- Global blood miRNA profiling unravels early signatures of immunogenicity of Ebola vaccine rVSVΔG-ZEBOV-GP.iScience · 2023Article
- Emodin protects against intestinal dysfunction and enhances survival in rat model of septic peritonitis through anti-inflammatory actions.Immunity, inflammation and disease · 2023Article
- A summary of the current diagnostic methods for, and exploration of the value of microRNAs as biomarkers in, sepsis-associated encephalopathy.Frontiers in neuroscience · 2023Review
- Neuronal exosomal miR-25-3p attenuates M1 microglial activation and neurotoxicity by targeting TLR4 to regulate the NF-κB signaling pathway.Frontiers in neurologyArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-associated encephalopathy (SAE) is a severe complication of sepsis. It has been reported that miR-25-3p is closely related to the development of sepsis. However, the detailed mechanism of miR-25-3p in SAE requires further investigation. Caecum ligation and puncture (CLP) was performed to induce SAE in vivo. LPS stimulation was applied to mimic the in vitro inflammatory model. The expression levels of TLR4 and NLRP3 in the cerebral cortex were evaluated by immunofluorescence. The gene and protein expression levels were determined by qRT-PCR and a western blot analysis. ELISA was used to detect the levels of inflammatory cytokines. The interaction between miR-25-3p and TLR4 was validated by a dual luciferase reporter assay. TLR4 and NLRP3 were highly expressed in the cerebral cortex of SAE mice, while miR-25-3p was expressed at low levels. Activation of the inflammasome, increased release of cytokines and microglial activation were also observed in the SAE mouse model. The overexpression of miR-25-3p inhibited the expression of LPS-induced cytokines and microglial activation. Furthermore, miR-25-3p inhibited TLR4 expression by directly targeting TLR4. The anti-inflammatory effect of miR-25-3p in LPS-induced CHME5 was reversed by TLR4 overexpression. miR-25-3p overexpression attenuated the activation of microglia in SAE by inhibiting the NLRP3/IL-1β/IL-18 axis by directly targeting TLR4, suggesting that miR-25-3p may be a potential target for SAE diagnosis and treatment.
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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 Socratic graph.