ArticleStroke and vascular neurology2026
Brain-targeted extracellular vesicles for anti-cuproptosis therapy in subarachnoid haemorrhage.
Article in Stroke and vascular neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Cuproptosis: New Mechanisms Linking Endothelial Dysfunction to Neurodegenerative Diseases and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential.Molecules (Basel, Switzerland) · 2026Review
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundSubarachnoid haemorrhage (SAH) is primarily caused by ruptured aneurysms with high mortality worldwide. Cuproptosis is a copper-induced cell death that regulates lipoylated tricarboxylic acid cycle proteins. The link between cuproptosis and SAH is unclear. To inhibit cuproptosis for SAH treatment, we designed brain-targeted delivery of siRNA to inhibit cuproptosis.
methodsTranscriptome data of SAH related to cuprotosis were extracted from the Gene Expression Omnibus and defined using quantitative reverse transcription-PCR. We injected RVG-RBCEVs/siRNA (rabies virus glycoprotein-red blood cell extracellular vesicles/siRNA) peripherally to deliver LIAS (lipoyl synthase) siRNA to the brain tissues of SAH mice. The influences of RVG-RBCEVs/siRNA on copper levels, enrichment of cuproptosis functional proteins, glutathione and malondialdehyde content, mitochondrial respiration and membrane potential, transmission electron microscope, a neurological score, brain water content, blood-brain barrier injury and Fluoro-Jade C staining were examined.
resultsOur findings revealed that three cuproptosis-related genes (CRGs) were differentially expressed. The RVG peptides were conjugated to the red blood cell extracellular vesicle surface by bio-orthogonal click chemistry reactions, and then the loading of siRNA was conducted. RVG-RBCEVs/siRNA was selectively taken up by neurons but not glial cells; it facilitated the downregulation of LIAS of CRGs, reduced the accumulation of reactive oxygen species, inhibited neuronal cuprotosis and exerted neuroprotective effects in vivo.
conclusionsThese findings suggest that cuprotosis is critical for inducing neural injury after SAH. Neuron-targeted RVG-RBCEVs/siRNA treatment attenuated oxidative stress by inhibiting cuproptosis via suppressed LIAS expression. This innovative approach alleviates neurobehavioural impairments and represents a neuroprotective strategy following SAH.
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