ArticleMetabolic brain disease2025
Suppression of miR-218 promotes SOCS3 expression to alleviate cognitive impairment and white matter injury after chronic cerebral hypoperfusion.
Article in Metabolic brain disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
- Roles of Microglia in Cerebral Small Vessel Disease.CNS neuroscience & therapeutics · 2026Review
- Temporal Evolution of Brain Inflammation in the Bilateral Common Carotid Artery Stenosis Model of Chronic Cerebral Hypoperfusion.Journal of inflammation research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic cerebral hypoperfusion-induced white matter injury (WMI) is a significant cause of vascular cognitive impairment. Emerging evidence suggests that miR-218 may be involved in the pathogenesis of WMI. However, understanding of the relationship between miR-218 and chronic hypoperfusion-induced WMI remains insufficient. Our study investigated the relationship between miR-218 and chronic hypoperfusion-induced WMI at clinical, animal, and cellular levels. We found that serum miR-218 expression was elevated in clinical WMI patients, had a certain diagnostic efficacy for WMI, and was correlated with the degree of WMI, cognitive scores, and serum inflammatory factors. In addition, we constructed a mouse model with bilateral carotid artery stenosis (BCAS) to simulate chronic hypoperfusion-induced WMI and detected an increase in miR-218 expression in the white matter of BCAS mice. Following administration of Lv-sh-miR-218 to the white matter of BCAS mice, improvements were observed in both cognitive impairment and WMI. Furthermore, Lv-sh-miR-218 also reduced M1 polarization of microglia and neuroinflammation within the white matter. Subsequently, we confirmed that SOCS3 is the specific target of miR-218 through bioinformatics analysis and luciferase reporter gene assays. Injection of LV-SOCS3 into the white matter also led to improvements in cognitive impairment and WMI in BCAS mice, along with reduced M1 polarization of microglia and neuroinflammation. Moreover, in primary cultured microglia cells, we demonstrated that after chronic hypoxia, miR-218 regulates inflammatory factors through the SOCS3/STAT3 pathway. In summary, our current results indicate a strong correlation between elevated miR-218 levels and chronic hypoperfusion-induced WMI, and downregulation of miR-218 expression can improve neuroinflammation by upregulating SOCS3, thereby ameliorating WMI and cognitive impairment.
Indexed as
Identifiers
40080253What 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.