ArticleNeural regeneration research2026
MicroRNA-200s attenuate demyelination caused by Angiostrongylus cantonensis in a mouse model by targeting phosphatase and tensin homolog.
Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed.
- Phosphatase and tensin homolog: A potential target for therapeutic intervention in optic nerve regeneration.Neural regeneration research · 2026Article
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JOURNAL/nrgr/04.03/01300535-202606000-00075/figure1/v/2026-02-11T151048Z/r/image-tiff Demyelinating diseases of the central nervous system are common, yet few effective strategies for myelin repair and remyelination are available. An increasing number of studies highlight the role of microRNAs (miRNAs) as key regulators of demyelination. miRNA mimics and inhibitors, which are currently in preclinical development, have shown promise as novel therapeutic agents. However, the mechanisms by which they protect myelin are not fully understood. Using a mouse model of acute central nervous system demyelination induced by infection with Angiostrongylus cantonensis , we investigated alterations in miRNA expression in the mouse brain. Our findings revealed a significant early-stage increase in the levels of miR-200, particularly miR-200a and miR-200c. Subsequent analysis demonstrated that combined miR-200a and miR-200c overexpression improved neurobehavioral outcomes and attenuated demyelination in Angiostrongylus cantonensis -infected mice. Further lipid metabolomic profiling indicated that miR-200a and miR-200c synergistically inhibited the production of phosphatase and tensin homolog (PTEN) and activated the phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin signaling pathway, as confirmed by double luciferase reporter assay and western blotting. Additionally, in vitro experiments showed that miR-200a and miR-200c protected oligodendrocyte precursor cells from lipopolysaccharide-induced damage and enhanced their survival. Our study indicates the critical role of miR-200a and miR-200c in protecting against central nervous system demyelination by targeting PTEN and modulating key survival pathways. Furthermore, our findings suggest that miR-200a and miR-200c are promising diagnostic biomarkers of and therapeutic targets for treating demyelination-related disorders.
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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.