# LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1

## TL;DR

This study shows that the lncRNA LINC01605 promotes aortic dissection by regulating smooth muscle cell functions through SGK1.

## Contribution

The novel contribution is identifying LINC01605 as a regulator of aortic dissection via its interaction with SGK1 in vascular smooth muscle cells.

## Key findings

- LINC01605 is upregulated in aortic dissection tissues and vascular smooth muscle cells.
- LINC01605 promotes VSMC proliferation, migration, and autophagy, especially under Ang II stimulation.
- LINC01605 targets SGK1 and its knockdown alleviates aortic dissection pathology in mice.

## Abstract

Long noncoding RNAs (lncRNAs) are emerging as key regulators in cardiovascular diseases. 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. Knockdown of LINC01605 alleviated AD pathology in mice, modulating synthetic phenotype and autophagy markers. LINC01605 plays an important role in AD. It regulates the function of VSMCs by targeting SGK1 and promotes the pathological process of AD. LINC01605 may be a potential target for AD treatment, providing new directions for the mechanism research and treatment strategies of AD.