Investigating the Role of Scd1 in OSAHS-Induced Vascular Changes

Abstract

This study investigates the role of Stearoyl-CoA Desaturase-1 (Scd1) in vascular remodeling associated with Obstructive Sleep Apnea-Hypopnea Syndrome (OSAHS) using multi-omics analysis. Transcriptomic and metabolomic datasets of OSAHS mouse models were analyzed to identify differentially expressed genes and metabolites, followed by functional enrichment analysis. Key genes were screened using weighted gene correlation network analysis (WGCNA) and machine learning, and a PPI network was constructed. An OSAHS mouse model was developed via intermittent hypoxia exposure. Human aortic smooth muscle cells (HASMCs) were subjected to hypoxia/reoxygenation cycles to simulate OSAHS in vitro. Blood pressure, plasma lipid profiles, histological changes in the thoracic aorta, and Scd1 protein expression were assessed. CCK-8 and Transwell assays evaluated HASMC proliferation and migration. Scd1 was identified as a critical factor in OSAHS-related vascular remodeling, with its expression significantly upregulated in vascular tissues of OSAHS mice. Metabolomic analysis revealed changes in fatty acid metabolism. Scd1 knockdown reduced blood pressure, lipid levels, aortic wall thickness, collagen deposition, elastic fiber accumulation, and mucin deposition in vivo. In vitro, hypoxia/reoxygenation cycles elevated Scd1 expression, while Scd1 knockdown inhibited HASMC proliferation and migration. Multi-omics analyses highlight Scd1 as a key regulator in OSAHS-associated vascular remodeling, driving pathological changes through its upregulation. These findings suggest Scd1 as a potential therapeutic target for managing OSAHS-related vascular pathologies.