ArticleCell communication and signaling : CCS2025
Targeting microglial NAAA-regulated PEA signaling counters inflammatory damage and symptom progression of post-stroke anxiety.
Article in Cell communication and signaling : CCS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Enhanced treatment of ischemic stroke by scutellarin loaded Angiopep-2-modified milk exosomes via multiple pathological pathways regulation.Journal of nanobiotechnology · 2026Article
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9 authors.
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Abstract
Post-stroke anxiety (PSA) manifests as anxiety symptoms after stroke, with unclear mechanisms and limited treatment strategies. Endocannabinoids, reported to mitigate fear, anxiety, and stress, undergo dynamic alterations after stroke linked to prognosis intricately. However, endocannabinoid metabolism in ischemic microenvironment and their associations with post-stroke anxiety-like behavior remain largely uncovered. Our findings indicated that endocannabinoid metabolism was dysregulated after stroke, characterized by elevated N-palmitoylethanolamide (PEA) hydrolase N-acylethanolamine-acid amidase (NAAA) in activated microglia from ischemic area, accompanied by rapid PEA exhaustion. Microglial PEA metabolite exhaustion is directly associated with more severe pathological damage, anxiety symptoms and pain sensitivity. Naaa knockout or pharmacological supplementation to boost PEA pool content can effectively promote stroke recovery and alleviate anxiety-like behaviors. In addition, maintaining PEA pool content in ischemic area reduces overactivated microglia by confronting against mitochondria dysfunction and inflammasome cascade triggered IL-18 release and diffusion to contralateral hemisphere. Meanwhile, maintenance of microglial PEA pool content in ischemic-damaged lesion can preserve contralateral vCA1 synaptic integrity, enhancing anxiolytic pBLA-vCA1
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