ArticleBiomaterials research2026
Intranasal Netrin-1 modRNA-Loaded Extracellular Vesicles Reduce Neuronal Apoptosis after Ischemic Stroke.
Article in Biomaterials research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Authors and funding
9 authors.
Funding
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Abstract
Ischemic stroke remains a leading cause of mortality and long-term neurological disability worldwide, while effective neuroprotective therapies remain limited. Netrin-1 is a multifunctional guidance molecule with neuroprotective properties, and chemically modified mRNA (modRNA) offers a promising platform for transient therapeutic protein expression. However, safe and efficient delivery of modRNA to the ischemic brain remains a major barrier to clinical translation. Here, we engineered Netrin-1 modRNA-loaded extracellular vesicles (EV@mNetrin-1) derived from human umbilical cord mesenchymal stem cells (hUMSCs) and administered them via a noninvasive intranasal route. EV-mediated delivery enabled intracellular translation of Netrin-1 modRNA into protein in neurons and increased Netrin-1 expression in ischemic brain tissue. In vitro, EV@mNetrin-1 significantly reduced neuronal apoptosis and improved neuronal survival following oxygen-glucose deprivation/reoxygenation (OGD/R). In vivo, intranasal administration of EV@mNetrin-1 enhanced brain Netrin-1 expression, reduced infarct volume, improved neurological outcomes, and attenuated neuronal apoptosis in transient middle cerebral artery occlusion (tMCAO) mice. Mechanistically, the neuroprotective effects of EV@mNetrin-1 were associated with DCC-dependent activation of PI3K/AKT signaling. Collectively, these findings demonstrate the therapeutic potential of intranasal EV-mediated Netrin-1 modRNA delivery for ischemic stroke and support the development of RNA therapeutics for central nervous system disorders.
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Registered trials
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