Abstract
BACKGROUND: Obstructive Sleep Apnea Hypopnea Syndrome (OSAHS), a common sleep-related breathing disorder, is closely associated with an increased risk of cardiovascular and metabolic comorbidities. Polysomnography, the diagnostic gold standard, is costly and environmentally sensitive. This study explored the diagnostic potential of miR-1180-3p and its role in Chronic Intermittent Hypoxia (CIH)-induced vascular injury. METHODS: Serum miR-1180-3p and CERS1 levels were measured in 112 OSAHS patients and 88 controls via qRT-PCR. Correlations with PSG parameters (LSpO₂, AHI, TS90%) were analyzed. In vitro, HUVECs were exposed to CIH, and miR-1180-3p effects on cell viability, apoptosis, and oxidative stress (MDA, SOD, GSH-Px) were assessed. TargetScan and dual-luciferase assays validated miR-1180-3p-CERS1 binding. Evaluating miR-1180-3p/CERS1 axis regulation of OSAHS pathogenesis via co-inhibition experiments. RESULTS: A significant upregulation of miR-1180-3p was detected in OSAHS patients (p < 0.001). miR-1180-3p served as an independent risk factor for OSAHS (OR = 5.405, 95% CI 2.247‒13.001) and held diagnostic value (AUC = 0.882). miR-1180-3p correlated negatively with LSpO(2) (r = -0.705) but positively with AHI (r = 0.676) and TS90% (r = 0.774), with correlations persisting across mild, moderate, and severe OSAHS subgroups. In CIH-treated HUVECs, miR-1180-3p inhibition restored cell viability, reduced apoptosis, and alleviated oxidative stress. CERS1 was confirmed as a direct target, and its silencing reversed miR-1180-3p inhibition-mediated protection. CONCLUSION: miR-1180-3p was a novel diagnostic biomarker for OSAHS. By targeting CERS1, miR-1180-3p exacerbated CIH-induced damage to HUVECs, thereby regulating the pathological progression of OSAHS.