ArticleFrontiers in genetics2026
miR-18a-5p promotes phenotypic transformation of airway smooth muscle cells by targeting SPRY1 to activate the RAS-MAPK pathway.
Article in Frontiers in genetics, 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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Abstract
Objective: This study investigates the role of miR-18a-5p in the phenotypic transformation of airway smooth muscle cells (ASMCs) and its underlying mechanism in asthma-related airway remodeling. Methods: Expression of miR-18a-5p in sputum from asthma patients was assessed by RT-qPCR. An Results: miR-18a-5p was significantly upregulated in asthma patients. Overexpression of miR-18a-5p promoted ASMC proliferation and migration, accompanied by upregulation of migration-related proteins (Integrin β1,p-FAK/FAK,p-Paxillin/Paxillin,MMP9), increased synthetic phenotype markers (α-SMA, OPN, Collagen I/III), and reduced contractile marker (Calponin). It also activated the RAS-MAPK pathway. SPRY1 was confirmed as a direct target of miR-18a-5p. Knockdown of SPRY1 reversed the effects of miR-18a-5p inhibition, confirming its role in mediating ASMC phenotypic changes. Conclusion: miR-18a-5p promotes ASMC phenotypic switching and airway remodeling in asthma by targeting SPRY1 and activating the RAS-MAPK signaling pathway. These findings suggest miR-18a-5p as a potential therapeutic target for asthma.
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