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pmid:41294029
LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1.
Mingliang Li · Ruonan Li · Zihe Zheng · Changbo Xiao · Quanlin Yang · Bo Chen · Xiaofu Dai
Journal of cellular and molecular medicine · 2025 doi:10.1111/jcmm.70963
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Complete file
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This study investigated the role of lncRNA LINC01605 in aortic dissection (AD) pathogenesis through its effects on vascular smooth muscle cells (VSMCs). Bioinformatics analysis of GEO datasets (GSE107844, GSE147026) identified LINC01605 as differentially expressed in AD. Its expression was validated in human aortic tissues and VSMCs using RT-qPCR and FISH. Functional assays (CCK-8, Transwell, Western blot) assessed VSMC proliferation, migration, phenotypic switching and autophagy. SGK1 was predicted as a target via bioinformatics and confirmed by RIP assays. Ang II-induced AD mice with LINC01605 knockdown were used for in vivo validation. LINC01605 was significantly upregulated in AD aortic tissues and VSMCs. Functional studies demonstrated that LINC01605 promoted VSMC proliferation, migration, invasion, phenotypic switching and autophagy, particularly under Ang II stimulation. Mechanistically, LINC01605 targeted SGK1 to regulate VSMC function. 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