ArticleJournal of extracellular vesicles2026
C1qc Mediates Blood-Brain Barrier Disruption in a Mouse Model of Intracerebral Haemorrhage Through Microglia-Derived Migrasomes.
Article in Journal of extracellular vesicles, 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
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Who cites it
1 citing paper in PubMed.
- C1qc Mediates Blood-Brain Barrier Disruption in a Mouse Model of Intracerebral Haemorrhage Through Microglia-Derived Migrasomes.Journal of extracellular vesicles · 2026Article
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Authors and funding
18 authors.
Funding
Abstract
Extracellular vesicles (EVs) are essential for intercellular communication and significantly influence neuroimmune responses after intracerebral haemorrhage (ICH). This study elucidates the immune mechanisms underlying secondary brain injury following ICH by identifying microglia-derived migrasomes. By integrating immune cell clustering analysis from single-cell RNA sequencing (scRNA-seq) with Mendelian randomization, we identified five key genes associated with ICH. Further experiments revealed that C1qc accumulates around hematomas, worsening blood‒brain barrier (BBB) disruption through migrasome-mediated pathways. Our results showed that microglial migrasomes transport C1qc to induce pyroptosis in vascular endothelial cells, thereby compromising BBB integrity. Genetic ablation of C1qc substantially attenuated this BBB damaging effect, C1qc-deficient migrasomes exhibited protective properties. Our findings, for the first time, reveal the mechanistic role of C1qc and migrasomes in ICH pathogenesis and establish microglia-derived migrasomes as promising therapeutic targets, providing novel avenues to improve neurologic outcomes after ICH.
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Registered trials
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