ArticleCells2023
Agomir-331 Suppresses Reactive Gliosis and Neuroinflammation after Traumatic Brain Injury.
Article in Cells, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed, 4 citations in OpenAlex.
- Evaluation of modafinil's neuroprotective effects in lipopolysaccharide-induced sepsis-associated encephalopathy: associations with GSK3β, inflammatory, oxidative stress, and apoptotic signaling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Role of microRNAs in major brain diseases, focusing on neuroinflammation and neuronal apoptosis.Iranian journal of basic medical sciences · 2026Review
- T7-Synthesized Double-Stranded RNA Mimicking miR-71 Induces Termite RNAi and Increases Fungal Efficacy.Biomolecules · 2025Article
- The Phenotype Changes of Astrocyte During Different Ischemia Conditions.Brain sciences · 2024Article
- Loss of microglial Arid1a exacerbates microglial scar formation via elevated CCL5 after traumatic brain injury.Cell communication and signaling : CCS · 2024Article
- Early-Stage Application of Agomir-137 Promotes Locomotor Recovery in a Mouse Model of Motor Cortex Injury.International journal of molecular sciences · 2023Article
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
Traumatic brain injury usually triggers glial scar formation, neuroinflammation, and neurodegeneration. However, the molecular mechanisms underlying these pathological features are largely unknown. Using a mouse model of hippocampal stab injury (HSI), we observed that miR-331, a brain-enriched microRNA, was significantly downregulated in the early stage (0-7 days) of HSI. Intranasal administration of agomir-331, an upgraded product of miR-331 mimics, suppressed reactive gliosis and neuronal apoptosis and improved cognitive function in HSI mice. Finally, we identified IL-1β as a direct downstream target of miR-331, and agomir-331 treatment significantly reduced IL-1β levels in the hippocampus after acute injury. Our findings highlight, for the first time, agomir-331 as a pivotal neuroprotective agent for early rehabilitation of HSI.
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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.