Exosome-related genes influence the progression of stroke through neuroinflammatory responses

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Ischemic stroke (IS) ranks among the top causes of mortality and disability globally. Exosomes exert a crucial effect on maintaining a complex regulatory balance with neuroinflammation in IS. Hence, this research aimed to elucidate the roles of exosome-related genes IS. We integrated data from five IS-related datasets from the Gene Expression Omnibus (GEO) database and exosome-related genes from ExoCarta. The least absolute shrinkage and selection operator regression and random forest models were performed to detect feature genes. Search Tool for the Retrieval of Interacting Genes and Cytoscape were employed to recognize the hub genes. Enrichment analyses were conducted to examine biological processes. CIBERSORT and MCPcounter were applied to assess immune infiltration, and Principal Component Analysis was utilized to explore the associations of feature genes and hub genes with immune cells. After identified different cell types, we analyzed differentiation, developmental trajectory, and interactions of the cell populations. Middle cerebral artery occlusion models were conducted on mice, followed by quantitative polymerase chain reaction to assess the expression levels of each hub gene. We identified 13 feature genes and 10 hub genes. Through qPCR, LGALS3, CD36, TLR2, ICAM1, and CD14 were significantly upregulated after Middle Cerebral Artery Occlusion surgery. Hub genes were s

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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